Four Days Session - Day 3 Updated - Presentation

BIOCHEMISTRY – A COMPLETE COURSE FOR NEET PG – DAY 3
Dr. C. SHANMUGAPRIYA
FATTY ACID SYNTHESIS
FACTS ABOUT FATTY ACID SYNTHESIS
• Cytoplasm
• Cytoplasm
• Acetyl CoA is the building block
• Cytoplasm
SOURCES OF ACETYL COA
malate
Prefffaffat
fyhnfA
OAA
TAtpunfp.ae
titrate
grit citate
FATES OF ACETYL COA
AUTEMREE
B
cholent
• Cytoplasm
• Acetyl CoA carboxylase is the rate limiting enzyme
SWA oh swA
JCB f of
Biotin Maligned
Au Bicarb
ATP
• Cytoplasm
• Acetyl CoA carboxylase is the rate limiting enzyme
• Fatty acid synthase complex is the other enzyme complex involved
FACTS ABOUT FATTY ACID SYNTHASE COMPLEX
Yoram 010
xp 910
7
00
THE
f
FACTS ABOUT FATTY ACID SYNTHASE COMPLEX
a
yyy gyy
yggg.gg pan MEECH cuz
co f
keoayesymayhpyen.ge rename
cys Gs 4
jan
Iffdffzketoaidpag m.mg
ffm
STEPS OF FATTY ACID SYNTHESIS
eye
In 9fEI24
adS
ianT
palmitic
STEPS OF FATTY ACID SYNTHESIS
2C
CoA
acetyl malefwa
1 2 NADPH
1 malonyl
CoA 2
Chf 1 ATPs
coa 12
acetyl
SUBUNITS OF FATTY ACID SYNTHASE COMPLEX
acid 16
palmitic 7 ATP
1HNADPH
WA 7 malonylCoA
acetyl
ER Throatian
ATA MTA KAS KAR Mychal
Acp
SUBUNITS OF FATTY ACID SYNTHASE COMPLEX
• Acetyl Transacylase
• Malonyl Transacylase
• Ketoacyl Synthase
• Ketoacyl reductase
• Hydratase
• Enoyl reductase
• Thioestaerase
• Acyl Carrier protein
REGULATION OF ACETYL COA CARBOXYLASE
• Stimulated by high energy
ATP
NADY
FADUZ
citrate
Invelli
• Stimulated by high energy ● Inhibited by low energy


• ATP
• NADH ADD
• FADH2 NAD
• Citrate
• Insulin
RAD
Alwyn
AcylWA
Amigaywide pgalactus

• ATP
• NADH ○ ADP
• FADH2 ○ NAD
• Citrate
• Bgalactoridas
Insulin ○ FAD
○ Acyl CoA
Kranked revolted ○ Glucagon
Dagestan
S.No PATHWAY RATE LIMITING ENZYMES
RATE LIMITING ENZYME
fify
FA Synthein AcetylCoA Carbylene
2
Is odour carnitine
3
Acyltryman I
Cholutie Synher HMGCoA reductase
4
Bile acid Syntten 7 α hydroxylase
5
keleiebodyfyretehnacotly.ae Synttare
S.No PATHWAY RATE LIMITING ENZYMES
RATE LIMITING ENZYME
1 Fatty Acid Synthesis Acetyl CoA carboxylase
2 Fatty Acid Oxidation Carnitine Acyl Transferase I
3 Bile Acid Synthesis 7 Alpha Hydroxylase
4 Ketone body synthesis HMG CoA Lyase
5 Cholesterol Synthesis HMG CoA reductase

• The precursor of fatty acids is
a. Propionyl CoA
b. Malonyl CoA
c. Acetyl CoA
d. Methyl Malonyl CoA
• The precursor of fatty acids is
a. Propionyl CoA
b. Malonyl CoA
c. Acetyl CoA
d. Methyl Malonyl CoA
• All the following are fates of acetyl CoA except
a. CO2
b. Ketone body
c. Cholesterol
d. Glucose
a. CO2
b. Ketone body
c. Cholesterol
d. Glucose
a. CO2
b. Ketone body
c. Cholesterol
d. Glucose
• The rate limiting enzyme of fatty acid synthesis is
a. HMG CoA reductase
b. HMG CoA Lyase
c. Acetyl CoA carboxylase
d. 7 Alpha hydroxylase
• The rate limiting enzyme of fatty acid synthesis is
a. HMG CoA reductase
b. HMG CoA Lyase
c. Acetyl CoA carboxylase
d. 7 Alpha hydroxylase
• All the following are requirements of Acetyl CoA carboxylase except
a. Bicarbonate
b. Biotin
c. ATP
d. NADH
• All the following are requirements of Acetyl CoA carboxylase except
a. Bicarbonate
b. Biotin
c. ATP
d. NADH
Q1 – All are true about Fatty acid synthase, EXCEPT :
a – It is Dimer
Yes
b – Acetyl CoA carboxylase is the first enzyme of the
complex
NO
c – Pantothenic acid is a component of the enzyme
d – It has got 7 enzmes, in each unit
Q1 – All are true about Fatty acid synthase, EXCEPT :
a – It is Dimer
b – Acetyl CoA carboxylase is the first enzyme of the
complex
c – Pantothenic acid is a component of the enzyme
d – It has got 7 enzmes, in each unit
Q2 – The most synthesized fatty acid by fatty acid
synthase complex is
a – Linoleic acid
b – Palmitic acid
c – Arachidonic acid
d – Stearic acid
Q2 – The most synthesized fatty acid by fatty acid
synthase complex is
a – Linoleic acid
b – Palmitic acid
c – Arachidonic acid
d – Stearic acid
Q3 – Lipogenesis is stimulated by all, EXCEPT :
a – High fatty diet
b – High Glucose diet You
Fetus
Fk
c – High Fructose based diet
Fr IP
d – Insulin
AldolaeB
DHAP
Aly
Motioned
93p
Q3 – Lipogenesis is stimulated by all, EXCEPT :
a – High fatty diet
b – High Glucose diet
c – High Fructose based diet
d – Insulin
CHOLESTEROL SYNTHESIS
FACTS ABOUT CHOLESTEROL SYNTHESIS
PHASE I 2Acetylen
Thiolace
acettaught
acetyloot una cossynman
UMANA
NADPH UMANA reductase R E
mevalonate
PHASE II mevalonate
CO2
Isoprenoid unite
PHASE III 6 Isoprenoid
d Dohill
Ubiquinone
cytepter I
Hene A
Squalene
PHASE IV Squalue
Squale Encore
I ER
Lenoriot
PHASE V Lanoste
Zymo
Dorno
cholecter
REGULATION OF CHOLESTEROL SYNTHESIS
REGULATION OF HMG COA REDUCTASE
• Allosteric Regulation
• Covalent Modification
• Allosteric Regulation Reloads
mevalonate Cholulet
• Induction or Repression
• Inhibited by all its products
• Mevalonate, Cholesterol and Bile acid
• Dephosphorylation
• Dephosphorylation
• Insulin induces in adipose tissue
REGULATION BY REPRESSION
GREY
SREBP
of
Ñm
sr
CHOLESTEROL SYNTHESIS – FACTS
• Cholesterol synthesis takes place in
a. Cytoplasm
b. Nucleus
c. Endoplasmic reticulum
d. a & c
• Cholesterol synthesis takes place in
a. Cytoplasm
b. Nucleus
c. Endoplasmic reticulum
d. a & c
Q1 – Statins act by inhibiting:
a – HMG CoA reductase
b – HMG CoA Lyase
c – Acetyl CoA carboxylase
d – 7 alpha hydroxylase
Q1 – Statins act by inhibiting:
a – HMG CoA reductase
b – HMG CoA Lyase
c – Acetyl CoA carboxylase
d – 7 alpha hydroxylase
Q1 – All the following are byproducts of cholesterol
synthesis except:
a – Dolichol
b – Ubiquitin
c – Heme A
d – Cholesterol
Q1 – All the following are byproducts of cholesterol
synthesis except:
a – Dolichol
b – Ubiquitin
c – Heme A
d – Cholesterol
FATTY ACID OXIDATION
FATTY ACID OXIDATION – FEW FACTS
FATTY ACID OXIDATION – FEW FACTS
• Mitochondria
• Very Long chain fatty acids get oxidised in peroxisome
• Very short chain fatty acids get oxidised in mitochondria
• Very short chain fatty acids get oxidised in mitochondria
• Short chain, medium chain and long chain fatty acids get oxidised in
both mitochondria and peroxisome
• β oxidation
FATTY ACIDS β
• CH3–CH2–CH2–CH2–CH2-CH2–CH2–CH2–CH2–CH2-CH3–CH2–CH2–CH2–CH2–CH2–CH2-COOH
nwHnaÑf
DIFFERENCE BETWEEN MITOCHONDRIAL AND
PEROXISOMAL OXIDATION
S.No PROPERTY MITOCHONDRIA PEROXISOME
1 Type of fatty acids USC SCMC LeFA SC MC LC VLCFA

2 Type of oxidation
β β
3 Products
Macelytcott 1 acetylCOA
4 ATP
NADU FADUD 4202
Ftp
DIFFERENCE BETWEEN MITOCHONDRIAL AND
PEROXISOMAL OXIDATION
S.No PROPERTY MITOCHONDRIA PEROXISOME
1 Type of fatty acids Very short, short, medium and Short, medium, long and very long chain
long chain fatty acid fatty acid
2 Type of oxidation β oxidation β oxidation
3 Products n/2 acetyl CoA n/2 acetyl CoA
4 ATP + No ATP, H2O2 peroxidation

FATE OF A FATTY ACID IN A CELL
pop T.FI
AMPtPPi
Acycot
symeten
carnitine
88
pays
NCA
ygyif.IT
FATE OF A FATTY ACID IN A CELL
FATTY ACID
Acyl CoA
ATP à AMP synthetase
Acyl CoA
CPT1
TAG
β
Cholesterol OXIDATION
Acyl CoA
ester
Acetyl CoA
HIGH LOW
ENERGY ENERGY
PHASES OF FATTY ACID OXIDATION
myfayot.pt
INCFA
I
t
02
Coz
10ATPO
• Phase I: n C fatty acids à n/2 acetyl CoA
• Phase I: n C fatty acids à n/2 acetyl CoA
• Phase II: Acetyl CoA gets into TCA cycle
STEPS OF BETA OXIDATION OF FATTY ACIDS
R Apr CoA
2 quSWA Acyl
CoAdehydrogenase
FATTY
1 EATRERADU Acyl
β mahatma
off foot
WHIP R
Yp Y
Hychatare
qNJ
COA β hycheryacyloot
2 FATEHLET BHAGWAdehydrogenase
f f
keoacylcot tw
uesAcelifecoA
o
STEPS OF BETA OXIDATION OF FATTY ACIDS
DETAILS OF PHASE I – EVERY CYCLE D
ENZYMES INVOLVED ENERGETICS PRODUCT
Acylcutdeelychger FADUZ 1 FATPS
hydrator AcetylCoA
BUAC delychogue NADH 2 KATPS 2C
Thiolone
4 ATPS
DETAILS OF PHASE I – EVERY CYCLE
ENZYMES INVOLVED ENERGETICS PRODUCT
Acyl CoA Dehydrogenase 4 Acetyl CoA
Hydratase
Beta Hydroxyacyl CoA

dehydrogenase
Thiolase
ENERGETICS OF BETA OXIDATION OF FATTY ACIDS
II
10 2
1 1 4 EX
ENERGETICS OF BETA OXIDATION OF FATTY ACIDS
10
1
1 4 2 2
1 1 4 8 40
80 2
28
1060
REGULATION OF CPT1
REGULATION OF CPT1
• STIMULATORS
REGULATION OF CPT1
• STIMULATORS ● INHIBITORS
WIFI M1A
NAD
FAD
Glucign
AcylevA
REGULATION OF CPT1
ii
• ADP
ATP
• NAD
• FAD FADUZ
• Glucagon Inulin
• Acyl CoA
yfA
y
E
FAsymi.TL Matron
REGULATION OF CPT1
• ADP ● ATP
• NAD ● NADH
● FADH2
• FAD
● Insulin
• Glucagon ● Malonyl CoA
• Acyl CoA
METABOLIC CHANGES IN DKA
www
Pgluxz
i
ii
e
METABOLIC CHANGES IN STARVATION
STEPS INVOLVED IN KETONE BODY SYNTHESIS
2Acetyler
Thiolan
acetoaeeytw acelje
funawtsynt
u
C.in acetoacetate
pursued
FACTS ABOUT KETONE BODY METABOLISM
FACTS ABOUT KETONE BODY METABOLISM
• Ketone bodies are products of incomplete fatty acid oxidation
• They are synthesised in diabetes and starvation because of low
availability of oxaloacetate
• Ketone bodies are synthesised in liver mitochondria
• Ketone bodies are utilised by extrahepatic tissues
• Liver can not utilise ketone bodies because they lack thiophorase or
succinyl CoA acetoacetate coA transferase
BIOCHEMICAL FEATURES OF FATTY ACID OXIDATION DEFECTS
Hypoglycemia FAO2
Non
keloticlynogeycemi FAcey.eu
LUNG
FA0 AA02 NHz
298kchemo
Decanguinidine
Dente Acquired
CATI
CATII Tamydipeddtime
ACD Misalpitddishier
Hydrant
BUALD
Tholeie
• Non ketotic hypoglycemia
• Hyperammonemia
• Dicarboxylic aciduria
ODD CHAIN FATTY ACID OXIDATION
Bovidalefs august 2th
ICFA
f acelytotffs
coA
3 FA Propinje
0
propionylCoA
Pc caryear
DmanyemalonylCoA
MM Racemare
MCQs Monytaratomi
Tenengmabyent acidimie
Adenyl Biz 11 MMM
of Badefania
Sueytwa
B12defining MMA Afli
an overjhe
fact
Q1 – Fatty acid Oxidation occurs in:
a – Mitochondria
b – Peroxisome
c – Both
d – None
Q1 – Fatty acid Oxidation occurs in:
a – Mitochondria
b – Peroxisome
c – Both
d – None
Q2 – Very short chain fatty acid Oxidation occurs in:
a – Mitochondria
b – Peroxisome
c – Both
d – None
Q2 – Very short chain fatty acid Oxidation occurs in:
a – Mitochondria
b – Peroxisome
c – Both
d – None
Q3 – Very long chain fatty acids undergo
a – β Oxidation
b – ω Oxidation
c – α Oxidation
d – γ Oxidation
Q3 – Very long chain fatty acids undergo
a – β Oxidation
b – ω Oxidation
c – α Oxidation
d – γ Oxidation
Q4 – Rate limiting enzyme of fatty acid oxidation:
a – Carnitine Acyl Transferase I
b – Carnitine Acyl Transferase II
c – Acyl CoA dehydrogenase
d – Thiolase
Q4 – Rate limiting enzyme of fatty acid oxidation:
a – Carnitine Acyl Transferase I
b – Carnitine Acyl Transferase II
c – Acyl CoA dehydrogenase
d – Thiolase
Q5 – How many cycles of beta oxidation does Palmitic
acid go through :
a–7
b–8
c–9
d – 16
Q5 – How many cycles of beta oxidation does Palmitic
acid go through :
a–7
b–8
c–9
d – 16
Q1 – CPT1 is activated by all, EXCEPT:
NEET
a – Acyl CoA
b – Malonyl CoA
c – High ADP/ATP ratio
d – Glucagon
Q1 – CPT1 is activated by all, EXCEPT:
a – Acyl CoA
b – Malonyl CoA
c – High ADP/ATP ratio
d – Glucagon
Q2 – Number of ATP generated in the liver by
complete oxidation of Palmitate:
a – 106
b – 33
c – 26
d – 16
complete oxidation of Palmitate:
a – 106
b – 33
c – 26
d – 16
complete oxidation of Stearic acid is:
a – 106
b – 120
c – 30
d – 26
complete oxidation of Stearic acid is:
a – 106
b – 120
c – 30
d – 26
ketosis is observed in Diabetes because of:
a – Low availability of oxaloacetate
b – Excess oxaloacetate
c – Low energy
d – Low fatty acid oxidation
ketosis is observed in Diabetes because of:
a – Low availability of oxaloacetate
b – Excess oxaloacetate
c – Low energy
d – Low fatty acid oxidation
Liver can not utilize ketone bodies because of lack
of:
a – Thiolase
b – Thioesterase
c – Thiophorase
d – Aconitase
Liver can not utilize ketone bodies because of lack
of:
a – Thiolase
b – Thioesterase
c – Thiophorase
d – Aconitase
Fatty acid oxidation defects present with all except:
a – Hypoglycemia
b – ketosis
c – Hyperammonemia
d – Dicarboxylic aciduria
Fatty acid oxidation defects present with all except:
a – Hypoglycemia
b – ketosis
c – Hyperammonemia
d – Dicarboxylic aciduria
HYPERLIPOPROTEINEMIAS
• Friedrickson’s Classification
• Six types
• Six types
• Type I
• Type IIa
• Type IIb
• Type III
• Type IV
• Type V
• Hypercholesterolemia
• Hypertriglyceridemia
annomas
• Hypercholesterolemia Tenden
atheoselem
ace
• Both
Tendon Xanthomas
• Hypercholesterolemia Accelerated
atherosclerosis
• Both
0000000
0 0
TENDON
XANTHOMAS
Tendon Xanthomas
atherosclerosis
Emptie
• Both tea panchalot
depend relate
Tendon Xanthomas
atherosclerosis
Eruptive Xanthomas
• Hypertriglyceridemia Recurrent Pancreatitis
Lipemia Retinalis
• Both
wᵈfE
follicilar lynerkeration
ERUPTIVE
XANTHOMAS
Tendon Xanthomas
atherosclerosis
Eruptive Xanthomas
• Hypertriglyceridemia Recurrent Pancreatitis
Lipemia Retinalis
• Both
• Both
• Hypercholesterolemia Type II a
• Both
• Hypercholesterolemia Familial
Type II a
Hypercholesterolemia
• Both
• Hypercholesterolemia Familial LDL receptor
Type II a
Hypercholesterolemia defect
• Both
Type II a
AUTOSOMAL
• Hypertriglyceridemia DOMINANT
• Both
Type II a
AUTOSOMAL
Type I, IV and V
• Both
Type II a
AUTOSOMAL
Type I, IV and V
• Both
Type IIb, III
TYPE I HYPERLIPOPROTEINEMIA
• Familial Hyperchylomicronemia syndrome
apoca LPL
eat
• Apo CII or LPL defect
E
• Hypertriglyceridemia 150cg1dL
• Recurrent pancreatitis, eruptive xanthomas
• Lipemia retinalis
• LPL activity is low
TYPE I HYPERLIPOPROTEINEMIA CAPOCH

• Apo CII or LPL defect iii in
plan
É
• LPL activity is low
• Post heparinised blood sample
LPL apocI
2P after mighty apocII
TYPE III HYPERLIPOPROTEINEMIA
• Apo E defect
are
• Apo E defect
• REMNANT DISEASE
• Apo E defect
• REMNANT DISEASE
• ELEVATION OF BOTH CHOLESTEROL & TGL
• Apo E defect
• REMNANT DISEASE
• BROAD BETA DISEASE
• Apo E defect
• REMNANT DISEASE
• FAMILIAL DYSBETALIPOPROTEINEMIA
LIPOPROTEIN ELECTROPHORESIS
1
-
- +
Are
- +
He
α
- +
ALPHA BAND /
HDL
- +
ALPHA BAND /
CHYLOMICRON HDL
- +
LIPOPROTEIN ELECTROPHORESIS LE LE
ALPHA BAND /
LpX
CHYLOMICRON HDL
- +
LCAT
DEFICIENCY
ALPHA BAND /
LpX HDL
- +
LIPOPROTEIN ELECTROPHORESIS 50
DISCOIDAL
LCAT HDL à
X
DEFICIENCY SPHEROIDAL
x
HDL ALPHA BAND /
LpX HDL
- +
DISCOIDAL
LCAT HDL à OBSTRUCTVE
DEFICIENCY SPHEROIDAL JAUNDICE
HDL ALPHA BAND
LpX
/ HDL
- +
ALPHA BAND
LpX / HDL
III
LDL
- +
ALPHA BAND
LpX / HDL
BETA/ Pre BETA

LDL BAND /VLDL
- +
ALPHA
LpX BAND / HDL
BETA/ Pre BETA

LDL BAND /VLDL
- +
ALPHA
LpX BAND / HDL
BROAD Pre BETA

BETA/ BAND /VLDL
- TYPE III
+
• Apo E defect
• REMNANT DISEASE
• Apo E defect
• REMNANT DISEASE 819
Ez Ez
• E2/E2
Palmer reupt
4 Sheerin
PALMAR ERUPTIVE
XANTHOMA palmoni
PALMAR ERUPTIVE
XANTHOMA
PALMAR ERUPTIVE PALMARIS XANTHOMA

XANTHOMA STRIAE
MCQS
• A 25 year old male presents with an episode of pancreatitis. His
cholesterol is 190mg/dL and Triglyceride level is 1180mg/dL. His
post heparinised Lipoprotein lipase activity is low. On mixing study,
the Lipoprotein lipase activity normalises. Which of the following is
true about his condition?
a.He will respond to fresh frozen plasma administration
b.It is a defect of Lipoprotein lipase
c.It is a defect of apo CIII
d.It is an autosomal dominant condition
• A 25 year old male presents with an episode of pancreatitis. His
cholesterol is 190mg/dL and Triglyceride level is 1180mg/dL. His
post heparinised Lipoprotein lipase activity is low. Which of the
following is true about his condition?
a.Broad beta band will be observed on lipoprotein electrophoresis
b.It is characerised by eruptive xanthomas
c.It is a defect of apo CIII XD yes
d.It is an autosomal dominant condition
• A 38 year old male presents with yellowish discoloration of palmar
creases as shown in the image. His cholesterol is 300mg/dL and
Triglyceride level is 280mg/dL. What is expected in his lipoprotein
electrophoresis?
a.A band at the site of application
b.Broad alpha band
c.Broad beta band
d.Absent alpha band
• A 38 year old male presents with yellowish discoloration of palmar
creases as shown in the image. His cholesterol is 300mg/dL and
Triglyceride level is 280mg/dL. What is expected in his lipoprotein
electrophoresis?
a.A band at the site of application
b.Broad alpha band
c.Broad beta band
d.Absent alpha band
GENETICS
ORGANISATION
8
ORGANISATION
TYPES OF NITROGENOUS BASES
● Two types
● Two types
● Purines
● Two types
● Purines
● Pyrimidines
● Two types
● Purines – 2 rings and 9 atoms
● Pyrimidines
● Two types
● Purines – 2 rings and 9 atoms
● Pyrimidines – 1 ring and 6 atoms

● Two types
● Purines
● Pyrimidines
● Two types
● Purines
● Pyrimidines C, U, T
● Two types
● Purines
● Pyrimidines C, U, T
Cytosine Uracil Thymine

NUCLEOSIDE
NUCLEOSIDE
• Base + Sugar à Nucleoside
NUCLEOSIDE
• Base + Ribose or Deoxyribose sugar à Nucleoside
ñ
1s
Leftridge
NUCLEOSIDE
no
• Base + Ribose or Deoxyribose sugar à Nucleoside + PO4 = NMP
PET
ALL 31
phosEster
NUCLEOSIDE
• NMP + PO4 = NDP
NUCLEOSIDE
• NMP + PO4 = NDP
• NDP + PO4 = NTP
STRUCTURE OF A NUCLEOTIDE
Me
ftp.nglyueeh
POLYNUCELOTIDE FORMATION
ftp.II
31
3’5’ PHOSPHODIESTER LINKAGE

O
LL
0
WATSON & CRICK MODEL
0 0 0
c
i
CHROMOSOME Hilton Bainprotein
Is Ilyin
J
iIIT
FACTS ABOUT HISTONES
I Ted
08
faddage
of
FF
FACTS ABOUT GENES to
do
Basset
Troubled
42N pyfgffnip.tl 7
fathom
finning.fr
IE iie
FACTS ABOUT GENES
DENATURATION 50
top Intact
1m
y
1m α salt
dualty Forward
TYPES OF DNA
B TYPE: Most common
Rt hardedy boiled
compleman
Cff
I mayer groo
3.44 bp
34 A
20A
feel team
1 mar grome
A TYPE:
Dehydration DNA RNA RNA RNA
Rt hauled loiter
11 tune
bp full
Grooves same dimension
Z TYPE:
ac seek stipe
Left hadedly
of 12 hp gut him
TYPES OF CHROMATIN
CHROMATIN
EUCHROMATIN HETEROCHROMATIN
CHROMATIN
HETEROCHROMATI
EUCHROMATIN
N
Active
CHROMATIN
Active
Uncondensed
CHROMATIN
Active
Uncondensed
Less densely
stained
CHROMATIN
Active Inactive
Uncondensed
Less densely
stained
CHROMATIN
Active
Uncondensed Inactive
Less densely condensed
stained
CHROMATIN
Active Inactive
Uncondensed condensed
Less densely More densely
stained stained
constitt facultat
CHROMATIN
CONSTITUTIVE
CHROMATIN
8K
CONSTITUTIVE FACULTATIVE
CHROMATIN
Banned
Always inactive
at e.g., Centromere
& Telomeres
CHROMATIN
Always inactive Occasionally

e.g., Centromere active
& Telomeres e.g., X
chromosome
PHASES OF CELL CYCLE
Go
Phase
Go G1
Phase Phase
S Phase
Go G1
Phase Phase
S Phase
Go G1 G2
Phase Phase Phase
S Phase
Go G1 G2
Phase Phase Phase
M Phase
S Phase
Go G1 G2
Phase Phase Phase
M Phase
S Phase
Go G1 G2
Phase Phase Phase
M Phase
S Phase
Go G1 G2
Phase Phase Phase
M Phase
S Phase
Go G1 G2
Phase Phase Phase
M Phase
S Phase
Go G1 G2
Phase Phase Phase
Complet
e resting M Phase
phase
S Phase
Go G1 G2
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED
CHROMOSOME
S Phase
Go G1 G2
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED
CHROMOSOME
S Phase
Go G1 G2
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
CHROMOSOME CHROMOSOME
Go
S Phase
Go G1 G2
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
REPLICATION
S Phase
Go G1 Timffman G2
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
REPLICATION
PROOFREADIN S Phase
G & REPAIR
Go G1 G2
pound
Phase Phase Phase pearls
Complet
e resting M Phase
phase
CONDENSED CONDENSED
REPLICATION
PROOFREADIN S Many
Phase
G & REPAIR
PROOFREADING
Go G1 G2
& REPAIR
Phase Phase Phase
e
Complet
e resting
phase to
M Phase
CONDENSED CONDENSED
REPLICATION
PROOFREADIN S Phase
G & REPAIR
PROOFREADING
Go G1 G2
& REPAIR
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
INTERPHASE
REPLICATION
PROOFREADIN S Phase
G & REPAIR
PROOFREADING
Go G1 G2
& REPAIR
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
UNCONDENSED
INTERPHASE
CHROMOSOME
REPLICATION
PROOFREADIN S Phase
G & REPAIR
PROOFREADING
Go G1 G2
& REPAIR
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
UNCONDENSED
INTERPHASE
CHROMOSOME
REPLICATION
PROOFREADIN S Phase
G & REPAIR
PROOFREADING
D
Go G1 G2
& REPAIR
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
CONDENSED FORM OF CHROMOSOME
v0
MI not you
manufactured
EfInfo
UNCONDENSATION OF CHROMOSOME
inD E A B
D FX
UNCONDENSED
INTERPHASE
CHROMOSOME
REPLICATION
PROOFREADIN S Phase
G & REPAIR
PROOFREADING
Go G1 G2
& REPAIR
Phase Phase Phase
Complet
e resting M Phase
phase
CONDENSED CONDENSED
MCQs
1. All of the following are purine bases except
a. Adenine
b. Uric acid
c. Hypoxanthine
d. Uracil.
1. All of the following are purine bases except
a. Adenine
b. Uric acid
c. Hypoxanthine
d. Uracil.
2. The linkage present in a nucleoside is
a. α N glycosidic linkage
b. β N glycosidic linkage
c. Phosphoester linkage
d. Acid anhydride linkage
2. The linkage present in a nucleoside is
3. The linkage present in a monophosphate nucleotide
is
3. The linkage present in a monophosphate nucleotide
is
5. The linkage present between individual nucleotides
in a polynucleotide chain is
a. 3’5’ phosphodiester linkage
d. 5’3’ phosphodiester linkage
5. The linkage present between individual nucleotides
in a polynucleotide chain is
a. 3’5’ phosphodiester linkage
d. 5’3’ phosphodiester linkage
tolerance
Ifs
1. Regarding DNA structure true is, K
a. The double helical structure is stabilised by
covalent bonds F
b. The individual strands are stabilized by 5’3’
phosphodiester linkage P
c. The individual strands are stabilized by 3’5’
phosphodiester linkage
Your
d. The term 5’ end indicates that the 5’ end is
linked to kinetochore. centromere
KINETOCHORE
1. Regarding DNA structure true is,
covalent bonds
linked to kinetochore.
1. Regarding DNA structure true is,
covalent bonds
linked to kinetochore.
• The histone that is not present is a nucleosome is
a. H1
b. H2A
c. H2B
d. H3
• The histone that is not present is a nucleosome is
a. H1
b. H2A
c. H2B
d. H3
12. Barr body is an example of
a. Euchromatin
b. Constitutive heteochromatin
c. Facultative heterochromatin
d. Hypersensitive heterochromatin
12. Barr body is an example of
a. Euchromatin
b. Constitutive heteochromatin
c. Facultative heterochromatin
d. Hypersensitive heterochromatin
2. The most common form of DNA is,
a. B DNA
b. Z DNA
c. A DNA
d. E DNA
2. The most common form of DNA is,
a. B DNA
b. Z DNA
c. A DNA
d. E DNA
3. The features of B DNA include, all except
a. It is a right handed helix
b. One full turn of DNA has 10 nuceotides and measure
34A0, width 20A0
c. Major groove is equal to minor groove in terms of
width
d. It is the form that is present under physiological
conditions.
3. The features of B DNA include, all except
a. It is a right handed helix
b. One full turn of DNA has 10 nuceotides and measure
34A0, width 20A0
c. Major groove is equal to minor groove in terms of
width
d. It is the form that is present under physiological
conditions.
4. The left handed helix is seen in,
a. B DNA
b. Z DNA
c. A DNA
d. E DNA
4. The left handed helix is seen in,
a. B DNA
b. Z DNA
c. A DNA
d. E DNA
• Denaturation of DNA is done by all except,
a. Increasing the temperature N
b. Increasing the salt concentration
c. Decreasing the salt concentration
d. Formamide
• Denaturation of DNA is done by all except,
a. Increasing the temperature
b. Increasing the salt concentration
c. Decreasing the salt concentration
d. Formamide
6. Which of the following is true?
a. To break AT bonds, high Tm is required
b. To break GC bonds, low Tm is required
c. To break AT bonds, low Tm is required
d. AT bonds and GC bonds need the same Tm
INICET NOV
2022
6. Which of the following is true?
a. To break AT bonds, high Tm is required
b. To break GC bonds, low Tm is required
c. To break AT bonds, low Tm is required
d. AT bonds and GC bonds need the same Tm
INICET NOV
2022
• Replication occurs in
a.Go Phase
b.G1 Phase
c.S Phase
d.M phase
• Replication occurs in
a.Go Phase
b.G1 Phase
c.S Phase
d.M phase
• The phase in which chromosomes are uncondensed is
a.Go Phase
b.G1 Phase
c.Metaphase
d.M phase
• The phase in which chromosomes are uncondensed is
a.Go Phase
b.G1 Phase
c.Metaphase
d.M phase
FACTS ABOUT TYPES OF HUMAN GENOMIC SEQUENCES
n of bp 3.3 109
ggengy.me 2ggyp
size of mrna 2000nA
Layout gene RBforel

doront
Layer poti Pitti Titu
More our genome Tito Lagat em
• Number of bp per human haploid genome is 3.3 X109
• Total number of genes identified 20 to 25000
• Average size of a gene is 27000bp
• Average size of mRNA 2000 nucleotides
• Largest gene is RBFox1
• Largest protein is Titin
• Gene with the largest exon is Titin
• Gene with the largest exon is Titin
• Gene with maximum number of exons is Titin
TYPES OF HUMAN GENOMIC SEQUENCES
Anthobacter luteus
8th May
I MIellaneus
Traiposon Jumpy get
Gene
Modent repute
IT 28 540
1001050 Ea.io
DNA
Enons Two 7 HRS
LINES SINES SSR
6 tomb 10082002ps
1
TYPES OF HUMAN GENOMIC SEQUENCES

• Three types
• CLASS I – 30% - GENE SEQUENCES

• 1.5% are coding exons
• 28.5% are non coding intervening sequences or introns
• CLASS II – 45% -TRANSPOSONS OR JUMPING GENES OR MODERATELY REPETITIVE

SEQUENCES (repeated between 1000 and lakh times)
• LINES or Long Interspersed Sequences (6 to 8 KB in length)
• SINES or Short Interspersed sequences (100 to 200 bp in length)
• CLASS III – 25% - MISCELLANEOUS SEQUENCES

• 3% is called as satellite DNA
HUMAN GENOME
SEQUENCES
GENE TRANSPOSONS MISCELLENEOUS
EXONS INTRONS LINES SINES HIV like
SATELLITE LSD ????

APPLICATIONS OF SATELLITE DNA
• Forensic application
• Forensic application
• To clear off paternal dispute cases
⑪
⑥
STEPS INVOLVED IN PATERNAL DISPUTE CASES
• Blood sample from mother, child and the suspected father
• DNA is extracted
IMSR 5 loci
• 5 MSR at 5 loci each at 227903141
• 5 MSR at 5 loci each
CHILD’S DNA – 8/8
MOTHER’S DNA – 11/8

MOTHER’S DNA – 11/8

MOTHER’S DNA – 11/8 FATHER’S DNA

MOTHER’S DNA – 11/8 FATHER’S DNA 11/10

MOTHER’S DNA – 11/8 FATHER’S DNA 11/10
NOT THE BIOLOGICAL FATHER

MCQs
• Alu family belongs to,
a. Unique non repetitive sequence
b. Moderately repetitive LINE sequence
c. Moderately repetitive SINE sequence
d. Highly repetitive sequence
• Alu family belongs to,
a. Unique non repetitive sequence
b. Moderately repetitive LINE sequence
c. Moderately repetitive SINE sequence
d. Highly repetitive sequence
A paternal dispute case was filed by a mother. The forensic centre
checked 5 VNTR systems.
INDIVIDUAL VNTR1 VNTR2 VNTR3 VNTR4 VNTR5
CHILD 9/10 8/11 10/12 9/8 6/7

MOTHER 7/9 8/9 11/10 9/11 6/9
Which of the following repeats should be observed in the putative

father's DNA for him to be considered as the biological father of the
child?
a. 7/8, 9/11, 11/12, 8/10,6/8
b. 7/8,9/11,10/12, 8/10, 6/8
c. 10/11, 11/10, 12/11, 8/7, 7/9
d. 10/11,11/10,11/10, 11/9, 9/10
A paternal dispute case was filed by a mother. The forensic centre
checked 5 VNTR systems.
INDIVIDUAL VNTR1 VNTR2 VNTR3 VNTR4 VNTR5
CHILD 9/10 8/11 10/12 9/8 6/7

MOTHER 7/9 8/9 11/10 9/11 6/9
Which of the following repeats should be observed in the putative

father's DNA for him to be considered as the biological father of the
child?
a. 7/8, 9/11, 11/12, 8/10,6/8
b. 7/8,9/11,10/12, 8/10, 6/8
c. 10/11, 11/10, 12/11, 8/7, 7/9
d. 10/11,11/10,11/10, 11/9, 9/10
REPLICATION
REPLICATION
REPLICATION
w w
0
DNA POLYMERASES
DNA POLYMERASES
• TEMPLATE STRAND
DNA POLYMERASES
• TEMPLATE STRAND
DNA POLYMERASES
• TEMPLATE STRAND
5’3’ POLYMERASE
ACTIVITY
5’ 3’
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
PRIMER
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
PRIMER dNTP
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
dNMP
PRIMER dNTP
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
dNMP
3’5’PDE
PRIMER dNTP
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
dNMP
3’5’PDE
PRIMER dNTP Magnesium

DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
dNMP
3’5’PDE
PRIMER dNTP Magnesium Buffer
e
DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’
dNMP 04113’
3’5’PDE

DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’
dNMP
3’5’PDE

DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’ 3’5’ exonuclease
dNMP
3’5’PDE activity

DNA POLYMERASES
• TEMPLATE STRAND
3’ 5’
5’3’ POLYMERASE
ACTIVITY
5’ 3’ 3’5’ exonuclease
dNMP
3’5’PDE activity
5’3’ exonuclease
activity
Ori
Ori
A-T
RICH i
e
Ori Ori
BP
A-T
RICH
Ori Ori
BP
A-T
RICH
REPLICATION
Ori Ori centre
BUBBLE
BP
A-T
RICH
STEPS OF REPLICATION
this pmi
goggaine
hagggshand
to
FUNCTIONS OF PROKARYOTIC DNA POLYMERASES
S.No DNA POLYMERASE FUNCTIONS
1 DNA Polymerase I Remove put preer fetteme gap
2 DNA Polymerase II
laggi stand eyatter
PR repair
3 DNA polymerase III
Leadig shard synhery Okazaki
fragments
FUNCTIONS OF PROKARYOTIC DNA POLYMERASES
1 DNA Polymerase I
2 DNA Polymerase II
3 DNA polymerase III

DIFFERENCES BETWEEN PROKARYOTIC & EUKARYOTIC GENOME
S.No PROKARYOTIC GENOME EUKARYOTIC GENOME

1 Smaller Larger
2
1 Smaller Larger
2 Closed circular Open linear

1 Smaller Larger
Multiple Ori s

1 Smaller Larger
Multiple Ori s

Telomeric end shortening
TELOMERIC END SHORTENING
m
we
2 deep Dope
RNA
v
TELOMERIC END SHORTENING

FUNCTIONS OF EUKARYOTIC DNA POLYMERASES
1 DNA Polymerase α
RNA primate
2 DNA Polymerase β
EII proof nepali
3 DNA polymerase ε
III Initiali leadyshard eywhein
4 DNA polymerase γ
Mt DNA Sylheti
5 DNA Polymerase δ
Couplets OkazakiPap Remover
fill the gap
1 DNA Polymerase α
2 DNA Polymerase β
3 DNA polymerase ε
4 DNA polymerase γ
5 DNA Polymerase δ
1 DNA Polymerase α RNA Primase
2 DNA Polymerase β Proof reading and repair
3 DNA polymerase ε Leading strand synthesis - Initiation
4 DNA polymerase γ Mitochondrial DNA synthesis
5 DNA Polymerase δ Completion of leading, Okazaki fragment
synthesis, Removes RNA primer and fills
the gap during lagging strand synthesis
MCQs
• Which of the following is true about replication?
a.Conservative process
b.Bidirectional
c.Non conservation
d.Unidirectional
• Which of the following is true about replication?
a.Conservative process
E
b.Bidirectional
c.Non conservation
d.Unidirectional
2. DNA polymerase requires all except,
a. RNA primer Yes
b. 3’ to 5’ strand to act as a templateYes
c. d NTP Yes
d. 5’ to 3’ strand as a template
2. DNA polymerase requires all except,
a. RNA primer
b. 3’ to 5’ strand to act as a template
c. d NTP
d. 5’ to 3’ strand as a template
3. Replication fork includes all except,
a. Helicase
b. Primase
c. DNA polymerase III
d. DNA polymerase I.
3. Replication fork includes all except,
a. Helicase
b. Primase
d. DNA polymerase I.
4. Replication along lagging strand, true is,
a. Polymerase I synthesizes along 3’ to 5’ direction
b. Helicase and primase join to form primosome and moves
along the lagging strand
c. Okazaki fragments are joined together by DNA helicase
d. DNA polymerase III removes RNA primer
4. Replication along lagging strand, true is,
a. Polymerase I synthesizes along 3’ to 5’ direction
b. Helicase and primase join to form primosome and moves
along the lagging strand
c. Okazaki fragments are joined together by DNA helicase
d. DNA polymerase III removes RNA primer
5. Function of DNA polymerase δ except,
a. Gap filling
b. Leading strand synthesis
c. Okazaki fragments synthesis
d. RNA primase
5. Function of DNA polymerase δ except,
a. Gap filling
b. Leading strand synthesis
c. Okazaki fragments synthesis
d. RNA primase
6. DNA polymerase with repair mechanism is:
a. DNA polymerase I
b. DNA polymerase II
β
d. DNA polymerase α
6. DNA polymerase with repair mechanism is:
a. DNA polymerase I
b. DNA polymerase II
d. DNA polymerase α
7. True about telomerase are all except:
a. They are present at the ends of eukaryotic chromosome Yes
b. Increased telomerase activity is associated with malignancy
c. DNA dependent RNA polymerase Yes
Ms
d. DNA polymerase
7. True about telomerase are all except:
a. They are present at the ends of eukaryotic chromosome
b. Increased telomerase activity is associated with malignancy
c. DNA dependent RNA polymerase
d. DNA polymerase
ERRORS OF REPLICATION
Bare Excuri
DNA ERRORS
DNA ERRORS
• Base excision error
2
EE
DNA ERRORS
• Mismatch error
DNA ERRORS
• Mismatch error
• Pyr Pyr Dimerisation
DNA ERRORS
• Mismatch error
• Ds DNA break
DNA ERRORS
• Base excision error – most common
• Mismatch error 11

• Ds DNA break
DNA ERRORS
undying
• Mismatch error - replication
• Ds DNA break
FEAST
DNA ERRORS
• Pyr Pyr Dimerisation – UV light
• Ds DNA break
DNA ERRORS
• Base excision error – most common nᵗ of
• Pyr Pyr Dimerisation – UV light
• Ds DNA break – Ionising radiation
FOUR REPAIR MECHANISM
• Base Excision Repair
• Mismatch repair
• Mismatch repair
• Nucleotide Excision repair
FOUR REPAIR MECHANISM MM HNPCD
• Mismatch repair
• Ds DNA break repair
Xewdena pimento
• Mismatch repair
It
Cockayne syndrome
• Mismatch repair
DS DNA BREAK
• Ionising radiation
DS DNA BREAK
• NHEJ (Non Homologous End Joining)

DS DNA BREAK
U X
• NHEJ (Non Homologous End Joining) ku

• HDR (Homologous DNA Repair)
DS DNA BREAK
• NHEJ (Non Homologous End Joining) Ku Helicase
• HDR (Homologous DNA Repair)

NHEJ - Ku HELICASE
NHEJ - Ku HELICASE
KU HELICASE
NHEJ - Ku HELICASE
KU HELICASE
NHEJ - Ku HELICASE
KU HELICASE
0
NHEJ - Ku HELICASE
KU HELICASE
NHEJ - Ku HELICASE
KU HELICASE
NHEJ - Ku HELICASE
KU HELICASE
NHEJ RESULTS IN LOSS

OF NUCLEOTIDE
SEQUENCES
E β
t
DEFECTS OF ds DNA BREAK REPAIR
•A
•B
•F
• ATAXIA TELANGIECTASIA
•B
•F
• BLOOM’S SYNDROME
•F
• FANCONI’S ANEMIA
NHEJ
NHEJ SCID
NHEJ SCID
• HBOC (Human Breast and Ovarian Cancer)

NHEJ SCID
HDR
• HBOC (Human Breast and Ovarian Cancer)
• The most common error in a DNA is
a.Base Excision
b.Pyrimidine dimer
c.Mismatch
d.Ds DNA break
• The most common error in a DNA is
a.Base Excision
b.Pyrimidine dimer
c.Mismatch
d.Ds DNA break
• Mismatch repair defect causes
a.HNPCC
b.Xeroderma pigmentosa
c.Fanconi’s anemia
d.Ataxia Telangiectasia
• Mismatch repair defect causes
a.HNPCC
b.Xeroderma pigmentosa
c.Fanconi’s anemia
d.Ataxia Telangiectasia
MUST KNOW MCQ
• UV light damage to the DNA leads to:
a. Purine dimers formed

b. DNA hydrolysis occurs
c. Specific endonuclease recognises the damage
d. Double stranded DNA break occurs
MUST KNOW MCQ
• UV light damage to the DNA leads to:
a. Purine dimers formed

b. DNA hydrolysis occurs
c. Specific endonuclease recognises the damage
d. Double stranded DNA break occurs
• Double stranded DNA break repair defect causes all
except
MMR
a. Hereditary Non polyposis Colon Cancer
b. Ataxia Telangiectasia
c. Bloom’s syndrome
d. Fanconi’s anemia
• Double stranded DNA break repair defect causes all
except
a. Hereditary Non polyposis Colon Cancer
b. Ataxia Telangiectasia
c. Bloom’s syndrome
d. Fanconi’s anemia
RNA, TRANSCRIPTION AND POST
TRANSCRIPTIONAL MODIFICATIONS
TYPES OF RNA
TYPES OF RNA
• rRNA
TYPES OF RNA
• rRNA
• mRNA
TYPES OF RNA
• rRNA
• mRNA
• tRNA
TYPES OF RNA
• rRNA
• mRNA
• tRNA
• sRNA
rRNA TIANA fos
f
tRNA yes 069
Ly ribozyme peptidylhayear
rRNA
GENE, TRANSCRIPTION, MODIFICATIONS
T
hhienemrva.rs prokaryotic
spley
No A tail addition
poly
7
RNA EDITING
APOBUS no
VLDL
Ayloneion
Hepatocytes
JUN TEAM
cytidmdiamiia
tsfust.mg mafioso
Urdie
Apo B48
Eta
C T
Apo B48
Apo B48
RNA EDITING
• Edit some of the nucleotide sequences of the fully formed mRNA in
specific tissues
RNA EDITING
specific tissues
• Aminoacids of the protein formed gets altered in some tissues

RNA EDITING
specific tissues
• Explanation for tissue specific regulation of gene expression

RNA EDITING
specific tissues
• Explanation for tissue specific regulation of gene expression
• Example is Apo B48 formation

tRNA - STRUCTURE
2 AA
50to1wR
AA
tRNA - STRUCTURE
3 II 51
Dawn
Ignition
aatrussyntretar .in Anticodon arm
tRNA - STRUCTURE glyFRNAsyntheter
pogey
fifthly
tRNA - STRUCTURE
sRNA
SnRNA
SiRNA
snRNA 6 lynes
Steinloop shuckier
v www
exckphie
fe
snRNA
• Six types – U1 to U7 except U3
• All except U7 help in splicing
• U7 helps in stem loop structure attachment
siRNA gene expression
FIT
t iE
3
siRNA
• Mediates interference of gene expression at the translation level
• One of the mechanisms of regulation of gene expression
• Causes gene knock down
MCQs
• m RNA is characterized by, all except
a. The nucleotide bases of mRNA are grouped in three to
form a codon.
b. Mature mRNA has a 7-methyl guanosine cap and poly A
tail
c. hn RNA is the form that is present in cytoplasm
d. hn RNA has introns in it
• m RNA is characterized by, all except
a. The nucleotide bases of mRNA are grouped in three to
form a codon.
b. Mature mRNA has a 7-methyl guanosine cap and poly A
tail
c. hn RNA is the form that is present in cytoplasm
d. hn RNA has introns in it
• Fidelity of gene is conferred by,
a. r RNA
b. m RNA
c. t RNA
d. Sn RNA
a. r RNA
b. m RNA
c. t RNA
d. Sn RNA
a. r RNA
b. aatRNA synthetase
c. t RNA
d. Sn RNA
a. r RNA
b. aatRNA synthetase
c. t RNA
d. Sn RNA
• The amino acid is attached to which arm
of tRNA
a. D arm
b. T ψ C arm
c. Acceptor arm
d. Anticodon arm
• The amino acid is attached to which arm
of tRNA
a. D arm
b. T ψ C arm
c. Acceptor arm
d. Anticodon arm
• Which of the following is the functions of D arm
of tRNA
a. Ribosomal attachment
b. Attachment of aatRNA synthetase
c. Aminoacid attachment
d. Anticodon arm
• Which of the following is the functions of D arm
of tRNA
a. Ribosomal attachment
b. Attachment of aatRNA synthetase
c. Aminoacid attachment
d. Anticodon arm
• The function of Sn RNA is
a. Formation of hn RNA
b. Formation of t RNA
c. Splicing
d. Formation of ribosomes.
• The function of Sn RNA is
a. Formation of hn RNA
b. Formation of t RNA
c. Splicing
d. Formation of ribosomes.
• siRNA causes
a. Gene knock down
b. Gene knock in
c. Gene Knock out
d. Gene conversion
• siRNA causes
a. Gene knock down
b. Gene knock in
c. Gene Knock out
d. Gene conversion
18. apo B 48 formation is an example of
a. Truncation of protein
b. RNA editing
c. Rearrangement of glycosidic bond
d. Modification by methylation
18. apo B 48 formation is an example of
a. Truncation of protein
b. RNA editing
c. Rearrangement of glycosidic bond
d. Modification by methylation
TRANSCRIPTION
REPLICATION AND TRANSCRIPTION
TEMPLATE STRAND IS PROVIDED
CODING STRAND IS PROVIDED
GENE IS PROVIDED
DNA & RNA POLYMERASES
DNA & RNA POLYMERASES
NUMBERING NUCLEOTIDES IN CODING STRAND
Band pometer Regulateentry
TRANSCRIPTION CONTROL REGIONS
Agulate
E 3
IE
5
a
PROMOTORS REGULATORS
Indidrepe
Enhancer
fidely frequency
INDUCERS
REPRESSORS
DPE
TATABO
Inr
18in
0
FIDELITY FREQUENCY
I RNA 9C CAAT
Polymerase
DIFFERENCES BETWEEN PROMOTOR AND
REGULATORS
S.No PROMOTOR REGULATOR
Baral Rgulates
1
Space seq TA Any
2
3
pattern
Onenteth
Meiji
4
hereapogie
5
lyly envened epact

specific
DIFFERENCES BETWEEN PROMOTOR AND
REGULATORS
S.No PROMOTOR REGULATOR
1 Sequence specific- TATA Box is active in No sequence specificity

human genome only when it is TATAAAG
2 Position specific – TATAAAG sequence is to be No position specificity. A regulator can act as a
present at -25th position in the coding strand regulator even if it is separated by a few 100
for it to be active nucleotides from the coding sequence
3 Orientation specific – TATAAAG is to be read No orientation specificity
that way when it is read from the 5’ end to
the 3’ end in the coding strand
4 Highly conserved, to some extent species Not conserved
specific
5 Not gene specific Tissue specific
11. Regarding transcription true is,
a. The two strands of DNA are transcribed stimultaneously
b. RNA primer is first formed
c. RNA polymerase needs the template strand in 5’ to 3’ direction
d. RNA polymerase synthesis the primary transcript in 5’ to 3’
direction
no
direction
Q. Template strand is 5’ CGTTATTTACTA3’. If this is transcribed by RNA
polymerase, the sequence of the new RNA will be
3 ATCAT
a. 5’GCAATAAATGAT3’
b. 5’GCAAUAAAUGAU3’
VAGUA
c. 5’UAGUAAAUAACG3’
d. 5’CGUUAUUUACUA3’
INICET MAY 2023

Q. Template strand is 5’ CGTTATTTACTA3’. If this is transcribed by RNA
polymerase, the sequence of the new RNA will be
a. 5’GCAATAAATGAT3’
b. 5’GCAAUAAAUGAU3’
c. 5’UAGUAAAUAACG3’
d. 5’CGUUAUUUACUA3’
INICET MAY 2023

direction
direction
12. A person admitted with the complaints of nausea and vomiting
following intake of mushroom in a party an hour before. A sample
of mushroom was obtained an it was found to be contaminated
with amanita phalloides. The RNA polymerase type
inhibited by this mushroom, which is responsible for these
symptoms is,
a. RNA polymerase I
b. RNA polymerase II
c. RNA polymerase III
d. RNA polymerase IV
12. A person admitted with the complaints of nausea and vomiting
following intake of mushroom in a party an hour before. A sample
of mushroom was obtained an it was found to be contaminated
with amanita phalloides. The RNA polymerase type
inhibited by this mushroom, which is responsible for these
symptoms is,
a. RNA polymerase I
b. RNA polymerase II
c. RNA polymerase III
d. RNA polymerase IV
13. True regarding promoter is,
a. It is gene specific
b. It is orientation non-specific
c. It is highly conserved species specificYes
d. TATA Box is the only promoter so far discovered
13. True regarding promoter is,
a. It is gene specific
b. It is orientation non-specific
c. It is highly conserved species specific
d. TATA Box is the only promoter so far discovered
14. True regarding regulators is,
a. They are required for basal expression
b. They are orientation specific
c. They should be located within a particularr distance, to be active
on a particular gene
d. They are cell specific
14. True regarding regulators is,
a. They are required for basal expression
b. They are orientation specific
c. They should be located within a particularr distance, to be active
on a particular gene
d. They are cell specific
15. Posttranscriptional modification of mRNA include all except
a.7- methyl guanosine capping
b. Poly A tail
2
c. Complete removal of introns
d. RNA editing
3 UTR
d D
UTR
15. Posttranscriptional modification of mRNA include all except
a.7- methyl guanosine capping
b. Poly A tail
c. Complete removal of introns
d. RNA editing
44
33
GENETIC CODE
4 64
Total no g coden 64
stop codons
Codas AA
PROPERTIES OF GENETIC CODE
• 61 codons
• 61 codons code for 20 aminoacids
• Degenerate
• Degenerate
• Exceptions methionine and Tryptophan

• Degenerate HE
• Unambiguous
11404507139
C
• Degenerate
• Unambiguous
• Non overlapping
• Degenerate
• Exceptions methionine and Tryptophan 11

• Unambiguous
• Non overlapping
• Not punctuated
• 61 codons code for 20 aminoacids 0910 stopcodon
• Degenerate
• Unambiguous
try
• Non overlapping
AAA AGG Ay
• Not punctuated
I
• Universal Stepcoder
WOBBLE PHENOMENON
WOBBLE PHENOMENON
• 5’ – GGG – GGC – GGA – GGU – 3’
31
58
47
70
I m t ane g rrna
WOBBLE PHENOMENON
• Reduced stringency when the 3rd nucleotide pair is formed between
codon and anticodon
WOBBLE PHENOMENON
codon and anticodon
• 3rd nucleotide of codon of mRNA is not specific

WOBBLE PHENOMENON
codon and anticodon
• 3rd nucleotide of codon of mRNA is not specific
• 1st nucleotide of anticodon of tRNA is not specific

TYPES OF MUTATION
Nt reg
AA seg
fn of protein
TYPES OF MUTATION
• Nucleotide Sequences
TYPES OF MUTATION
• Aminoacid sequences
TYPES OF MUTATION
• Aminoacid sequences
• Function of protein
TYPES OF MUTATION - Nucleotide Sequences
t FS Mulate
point meetate
Substitution
tf
IT Dolet Inverter
Transiter transverse
puts pu puts pyr
py Pyo
TYPES OF MUTATION - Aminoacid Sequences
Line
17 Noneme
AA Chaged C A
AAreq c Al stopcoden
C A C2 Az
cat
TYPES OF MUTATION – Function of protein
Tannty
Accepted
Ntieg
aceepletic
immedecht
Ntrey AAreqx
UB AAreq fnqprote
67MAA svalue.th Noli
Life
Hb Milwaukee 4b
Hb BristolApe
ub Sydney
6ᵗʰ coden Glu
Val
MCQs
s
2. No of possible codons
a. 64
b. 61
c. 20
d. 31
2. No of possible codons
a. 64
b. 61
c. 20
d. 31
3. No of codons which code for an aminoacid
a. 64
b. 61
c. 20
d. 31
3. No of codons which code for an aminoacid
a. 64
b. 61
c. 20
d. 31
4. Codon consists of:
a. 3 base pairs
b. 2 base pairs
c. 5 base pairs
d. 3 nucleotides
4. Codon consists of:
a. 3 base pairs
b. 2 base pairs
c. 5 base pairs
d. 3 nucleotides
4. Stop codon:
a. UAG
b. UCA
c. UAC
d. AUG
4. Stop codon:
a. UAG
b. UCA
c. UAC
d. AUG
5. All the following are properties of genetic code except,
a. Degenerate
b. Ambiguous
c. Nonoverlapping
d. Universal
5. All the following are properties of genetic code except,
a. Degenerate
b. Ambiguous
c. Nonoverlapping
d. Universal
5. The amino acid which does not follow degeneracy of codon is,
a. Glycine
b. Glutamine
c. Tryptophan
d. Tyrosine
5. The amino acid which does not follow degeneracy of codon is,
a. Glycine
b. Glutamine
c. Tryptophan
d. Tyrosine
6. Wobble phenomenon explains which of the following,
a. Degeneracy
b. Unambiguity
c. Ambiguity
d. Punctuation
6. Wobble phenomenon explains which of the following,
a. Degeneracy
b. Unambiguity
c. Ambiguity
d. Punctuation
CASE BASED MCQs
• A 45 year old male is detected to have fasting and postprandial
hyperglycemia in the diagnostic range of diabetes. To understand
his long term glycemic control, he is asked to estimate his HbA1C.
Chromatogram detects an abnormal Hemoglobin peak,
corresponding to Hb Bristol. His oxygen carrying capacity is
normal. Hb Bristol is an example of
a. Silent Mutation
b. Acceptable mutation
c. Partially acceptable mutation
d. Non sense mutation
• A 45 year old male is detected to have fasting and postprandial
hyperglycemia in the diagnostic range of diabetes. To understand
his long term glycemic control, he is asked to estimate his HbA1C.
Chromatogram detects an abnormal Hemoglobin peak,
corresponding to Hb Bristol. His oxygen carrying capacity is
normal. Hb Bristol is an example of
a. Silent Mutation
b. Acceptable mutation
c. Partially acceptable mutation
d. Non sense mutation
STEPS OF TRANSLATION
INITIATION
PIF
INITIATION
• eIF
INITIATION
• eIF
2
Meet
0
• eIF2C
INITIATION
• eIF
tRNA Methionine complex
• eIF2C formation
INITIATION
• eIF
• eIF2C
• eIF3 & 1A
INITIATION
• eIF
• eIF2C
• eIF3 & 1A
• eIF 4G/4A
INITIATION
• eIF
• eIF2C
• eIF3 & 1A
• eIF 4G/4A
• eIF4A/4B
INITIATION
• eIF
O
• eIF2C
• eIF3 & 1A
• eIF 4G/4A
• eIF4A/4B
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF3 & 1A
• eIF 4G/4A
• eIF4A/4B
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF3 & 1A Stabilise 40s ribosome
• eIF 4G/4A
• eIF4A/4B
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF 4G/4A Guides mRNA cap to ribosome
• eIF4A/4B
AB
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF4A/4B ATP dependent helicase
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF5 Removes 3 & 1A

proleey
sweetener 0 0
on
xo0m n
PA
819A HAHB
etgcʰTP 4914A
43s
3
5 Bet PU
TELEEL
Meet
2
Q HÉ
s tha
o
Bet
STEPS OF TRANSLATION 3
m
000
EFIA9
f
P
IIIIIIniffing paradigetranger
EF.IE
RI9TP
4 34 1 4 1
t
INITIATION
• eIF
• eIF2C
• eIF3 & 1A
• eIF 4G/4A
• eIF4A/4B
• eIF5
INITIATION
• eIF
• eIF2C formation
• eIF5 Removes 3 & 1A

ENERGETICS OF TRANSLATION
S.No STEP Number of ATPs
1
2
3
TOTAL
ENERGETICS OF TRANSLATION
S.No STEP Number of ATPs
1 Activation of aminoacid 2
2 Attachment of aatRNA to A site 1
3 Translocation step 1
TOTAL 4
DIFFERENCES BETWEEN imet tRNA & OTHER tRNAs
S.No imet tRNA aa tRNA
1
2
3
DIFFERENCES BETWEEN imet tRNA & OTHER tRNAs
S.No imet tRNA aa tRNA
1 Guided by eIF2C Guided by eEF1A

2 Attached to P site of 60 s Attached to A site of 60 s ribosome
ribosome
3 3 high energy phosphates are 4 high energy phosphates are required

required
TRANSLATION INHIBITORS
S.No
INHIBITORS LIST
INHIBITOR
we
T Sadabad
MECHANISM OF ACTION
1
Freezes into
2
Aminoglycoside Poynne
3 Tetracycline EFIA aatra A
chloramphenicol prokaryote
4 pentatyehayarae
5 Cycloheren
Ruin Eukaryote
Mandide clindamycin Translocation prokaryote
6
Eukaryotes Tranlocution
7
Tffonger aatra
analyn
INHIBITORS LIST
S.No INHIBITOR MECHANISM OF ACTION
1 Aminoglycosides All steps – freeze initiation, inhibit polysome formation
2 Tetracycline EF1A – inhibits attachment of aminoacyl tRNA to A site
3 Chloramphenicol 23srRNA or prokaryotic peptidyl transferase
4 Cycloheximide & Ricin Eukaryotic peptidyl transferase
5 Macrolide and clindamycin Prokaryotic translocation
6 Diphtheria and Pseudomonas toxin Eukaryotic translocation
7 Puromycin aatRNA analogue causes premature termination of protein

synthesis
INHIBITORS LIST - MNEMONIC
• BUY AT 30 AND CCEL AT 50

• BUY AT 30 AND CCEL AT 50

• Aminoglycosides
• Tetracycline
• Chloramphenicol
• Clindamycin
• Erythromycin
• Linezolid
MCQs
1. P and A sites are components of
a. 80s
b. 40s
c. 60s
d. 30s
1. P and A sites are components of
a. 80s
b. 40s
c. 60s
d. 30s
2. The function of shine Dalgarno sequence is to
a. Identify the termination signal
b. Help in guiding mRNA to ribosome
c. Identify initiation codon
d. Dissociate ribosome
2. The function of shine Dalgarno sequence is to
a. Identify the termination signal
b. Help in guiding mRNA to ribosome
c. Identify initiation codon
d. Dissociate ribosome
3. The translation factor which guides aatRNA to A site is
a. eIF1A
b. eEF4A
c. eEF1A
d. eIF3
3. The translation factor which guides aatRNA to A site is
a. eIF1A
b. eEF4A
c. eEF1A
d. eIF3
4. The total number of ATPs required for
attaching every aminoacid to a growing
polypeptide chain is
a. 1
b. 2
c. 3
d. 4
attaching every aminoacid to a growing
polypeptide chain is
a. 1
b. 2
c. 3
d. 4
forming a polypeptide chain with n
aminoacids is
a. 4n-1
b. 4n+1
c. 3n
d. 4n
forming a polypeptide chain with n
aminoacids is
a. 4n-1
b. 4n+1
c. 3n
d. 4n
9. mettRNA is attached to
a. P site of 40s ribosome
b. A site of 40s ribosome
c. P site of 60s ribosome
d. A site of 60s ribosome
9. mettRNA is attached to
a. P site of 40s ribosome
b. A site of 40s ribosome
c. P site of 60s ribosome
d. A site of 60s ribosome
10. The step which does not require high energy
phosphate is,
a. met tRNA synthesis
b. Aminoacyl tRNA synthesis
c. Peptide bond formation
d. Termination
10. The step which does not require high energy
phosphate is,
a. met tRNA synthesis
b. Aminoacyl tRNA synthesis
c. Peptide bond formation
d. Termination
11. Peptidyl transferase true are all except
a. It is a protein
b. It is an RNA
c. It does not require high energy phosphate
d. It is inhibited by chloramaphenicol
11. Peptidyl transferase true are all except
a. It is a protein
b. It is an RNA
c. It does not require high energy phosphate
d. It is inhibited by chlormaphenicol
12. Tetracycline inhibits
a. IF1A
b. EF1A
c. IF2C
d. EF2C
12. Tetracycline inhibits
a. IF1A
b. EF1A
c. IF2C
d. EF2C
13. Ricin inhibits
a. aatRNA synthetase
b. Peptidyl transferase
c. Termination
d. Initiation
13. Ricin inhibits
a. aatRNA synthetase
b. Peptidyl transferase
c. Termination
d. Initiation
14. Diphtheria toxin inhibits
a. IF1A
b. EF1A
c. IF2C
d. EF2
14. Diphtheria toxin inhibits
a. IF1A
b. EF1A
c. IF2C
d. EF2
15. Macrolide inhibits
a. Peptide bond formation
b. Termination
c. Translocation
d. Initiation
15. Macrolide inhibits
a. Peptide bond formation
b. Termination
c. Translocation
d. Initiation
• A 25 year old male presents with a skin infection with yellowish
crusts on the face. Impetigo was diagnosed and was prescribed
Mupirocin ointment. Mupirocin acts by
a. Inhibiting the binding of RNA polymerase to +1 site
b. Causing premature termination of mRNA synthesis
c. Causing premature termination of protein synthesis
d. Inhibiting translocation of ribosomes
• A 25 year old male presents with a skin infection with yellowish
crusts on the face. Impetigo was diagnosed and was prescribed
Mupirocin ointment. Mupirocin acts by
a. Inhibiting the binding of RNA polymerase to +1 site
b. Causing premature termination of mRNA synthesis
c. Causing premature termination of protein synthesis
d. Inhibiting translocation of ribosomes
IMAGE BASED MCQs
X
Name X shown in the blue box,
given the clue that it is an
antibiotic, which inhibits the blue
circle shown in the image.
a. Puromycin
b. Macrolide
c. Clindamycin
d. Chloramphenicol
X
Name X shown in the blue box,
given the clue that it is an
antibiotic, which inhibits the blue
circle shown in the image.
a. Puromycin
b. Macrolide
c. Clindamycin
d. Chloramphenicol
THANK YOU

Four Days Session - Day 3 Updated - Presentation

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Four Days Session - Day 3 Updated - Presentation

Uploaded by

Copyright:

Available Formats

BIOCHEMISTRY – A COMPLETE COURSE FOR NEET PG – DAY 3

• Stimulated by high energy

• Stimulated by high energy ● Inhibited by low energy

• Stimulated by high energy ● Inhibited by low energy

• Stimulated by high energy ● Inhibited by low energy

Kranked revolted ○ Glucagon

1 Fatty Acid Synthesis Acetyl CoA carboxylase

2 Fatty Acid Oxidation Carnitine Acyl Transferase I

3 Bile Acid Synthesis 7 Alpha Hydroxylase

4 Ketone body synthesis HMG CoA Lyase

5 Cholesterol Synthesis HMG CoA reductase

1 Type of fatty acids USC SCMC LeFA SC MC LC VLCFA

3 Products n/2 acetyl CoA n/2 acetyl CoA

4 ATP + No ATP, H2O2 peroxidation

Acylcutdeelychger FADUZ 1 FATPS

Acyl CoA Dehydrogenase 4 Acetyl CoA

Beta Hydroxyacyl CoA

• Non ketotic hypoglycemia

• Familial Hyperchylomicronemia syndrome

BETA/ Pre BETA

BETA/ Pre BETA

BROAD Pre BETA

PALMAR ERUPTIVE PALMARIS XANTHOMA

● Purines – 2 rings and 9 atoms

● Purines – 2 rings and 9 atoms

● Pyrimidines – 1 ring and 6 atoms

Cytosine Uracil Thymine

3’5’ PHOSPHODIESTER LINKAGE

WATSON & CRICK MODEL

Always inactive Occasionally

Layout gene RBforel

TYPES OF HUMAN GENOMIC SEQUENCES

• CLASS I – 30% - GENE SEQUENCES

• CLASS II – 45% -TRANSPOSONS OR JUMPING GENES OR MODERATELY REPETITIVE

• CLASS III – 25% - MISCELLANEOUS SEQUENCES

GENE TRANSPOSONS MISCELLENEOUS

EXONS INTRONS LINES SINES HIV like

SATELLITE LSD ????

MOTHER’S DNA – 11/8

MOTHER’S DNA – 11/8

MOTHER’S DNA – 11/8 FATHER’S DNA

MOTHER’S DNA – 11/8 FATHER’S DNA 11/10

MOTHER’S DNA – 11/8 FATHER’S DNA 11/10

NOT THE BIOLOGICAL FATHER

INDIVIDUAL VNTR1 VNTR2 VNTR3 VNTR4 VNTR5

CHILD 9/10 8/11 10/12 9/8 6/7

Which of the following repeats should be observed in the putative

INDIVIDUAL VNTR1 VNTR2 VNTR3 VNTR4 VNTR5

CHILD 9/10 8/11 10/12 9/8 6/7

Which of the following repeats should be observed in the putative

PRIMER dNTP Magnesium

PRIMER dNTP Magnesium Buffer

PRIMER dNTP Magnesium Buffer

PRIMER dNTP Magnesium Buffer

PRIMER dNTP Magnesium Buffer

PRIMER dNTP Magnesium Buffer

1 DNA Polymerase I Remove put preer fetteme gap

3 DNA polymerase III

S.No PROKARYOTIC GENOME EUKARYOTIC GENOME

S.No PROKARYOTIC GENOME EUKARYOTIC GENOME

S.No PROKARYOTIC GENOME EUKARYOTIC GENOME

2 Closed circular Open linear

S.No PROKARYOTIC GENOME EUKARYOTIC GENOME