CELL DIVISION (MITOSIS)
 Division of somatic cell that result in 2
genetically identical daughter cells
 Cells must divide for growth, repair and
asexually reproduce
 Begins in Interphase, when chromosomes
duplicate
 Daughter cells are genetically identical to parent
cell with same kind and number of
chromosomes
 Mitosis occurs in somatic or body cells (ex.
Liver, stomach, heart etc.)
 Chromosomes are called as DIPLOID which is
the total number of chromosomes in a somatic
cell
DIPLOID means “2 sets” and written as “2N”
 Body cells od adult organisms have 2 sets of
homologous (matching) chromosomes- 1 set
from female parent and 1 set from male parent
BODY CELLS AND GAMETES
BODY CELLS
 Also called as somatic cells
GERM CELLS
 Develops into gametes
 Located in the ovaries and testes
 Identified as sex cells
 Have DNA that can be passed to offspring
AUTOSOMES AND SEX CHROMOSOMES
 Body cells 23 pairs of chromosomes;
HOMOLOGOUS pairs of chromosomes
(same structure)
 Each homologous pair one chromosome
comes from each parent
 Chromosome pair 1-22 are autosomes
 Sex chromosomes, X and Y determine
gender in mammals
BODY CELLS (diploid)
GAMETES (haploid)
 Fertilization between egg and sperm occurs
in sexual reproduction
 Diploid (2n) cells have two copies of every
chromosomes.
 Body Cells are diploid
 Half the Chromosomes come from
each parent.
 Haploid (n) cells have one copy of every
chromosomes
 Gametes are haploid
 Gametes have 22 autosomes and 1
sex chromosome
CELL DIVISION (MEIOSIS)
 Number of chromosomes in the
original cell is reduced by half through
the separation of homologous
chromosomes
 Occurs in sex organs only
 MALES (XY)-sex organs are the testes
 FEMALES (XX)-sex organs are the ovaries
TWO STAGES:
1. MEIOSIS I (Reductional Division)
2. MEIOSIS II (Equational Division)
Meiosis produces sex cells – Cells with ½ the
number of chromosomes as the original cell
 Males – produces 4 sperm
 Females – produces 1 (viable) egg
The other 3 cells are called polar bodies – they
give up their cytoplasm to nourish the 1 good egg
 Gametes (sex cells; egg and sperm)
 Haploid (half number of chromosomes as
somatic (body) cells. Haploid means “1
set” and is written as “N”
 ANIMAL DIPLOID HAPLOID UNIQUE EVENTS IN MEIOSIS
HUMAN 46 23  HOMOLOGOUS (matching) chromosomes
DOG 78 39 pair up before 1st cell division
FLY 8 4
 Looks alike
 Code for same traits
 Receive one from each parent

HAPLOID CELLS MATURE INTO MATURE

GAMETES
 Gametogenesis is the production of
gametes; female and male gametogenesis
differ.
 Sperm become streamlines and
motile
 Sperm primarily contribute DNA to an
embryo
 Eggs contribute DNA, cytoplasm and
organelles to an embryo; during
meiosis the egg gets most of the
contents; the other cells form polar
bodies.
WHEN DOES MEIOSIS OCCUR IN HUMANS?
1. MALES (puberty)
2. FEMALES (before birth)
 all eggs are produced before birth and at
puberty eggs mature
MEIOSIS
 Sex cells divide produces gametes
 Gametes have half number of
chromosomes
 Occurs in GONADS (testes or ovaries)
MALE (spermatogenesis)
FEMALE (oogenesis)
“ MEIOSIS also shuffles the genes so that an
individual’s gametes are genetically different from
one another”
GENETIC SHUFFLING OF MEIOSIS I
1. CROSSING OVER (prophase I)
2. INDEPENDENT ASSORTMENT
(metaphase I)
INTERPHASE I
 Similar to Mitosis interphase
 Chromosomes replicate (S phase)
 Each duplicated chromosome consist of two
identical sister chromatids attached at their
centromeres
 Centriole pairs also replicate

MEIOSIS I
 Reductional division
 Reduces chromosomes by ½
 4 phases (PMAT I)

PROPHASE I
 Longest and most complex phase (90%)
FERTILIZATION (process by which egg and sperm  Divided into 5 stages (LE, ZA, PA, DI, DIA)
unite)  Leptotene
ZYGOTE (fertilized egg)  Zygotene
EMBRYO (organism in early stage of development)
 Pachytene
 Diplotene
 Diakinesis
  Chromosomes condense
 SYNAPSIS occurs; homologous
chromosomes come together to form a
tetrad
 TETRAD is two chromosomes or four
chromatids (sister or non-sister) overlap
PROPHASE I: LEPTOTENE or LEPTONEMA
 All chromosomes begin to condense
 Increase in nuclear volume
 Homology search (essential for initial pairing
of homologs)
PROPHASE I: ZYGOTENE or ZYGONEMA
 Pairing between homologus chromosome
and ends with complete pairing
 SYNAPSIS (homologous dyad)
 Process of pairing (at end to end)
between homologus chromosomes
 Synaptonemal complex is formed
 At completion; paired homologs take the
form of bivalents.
The number of bivalents is equal to the haploid
number
SYNAPTONEMAL COMPLEX (SC)
 A ladder like structure with transverse
protein filaments connecting the two lateral
elements
BIVALENT/TETRAD
 Complex forms by a synapsed homologous
chromosomes
HOMOLOGOUS CHROMOSOME
 Pair of chromosomes (maternal and
paternal) that are similar in shape and size.
 Homologous pairs (tetrads) carry genes
controlling the same inherited traits.
 Each locus (position of a gene) is in the
same position on homologues.
 Human have 23 pairs of homologous
chromosomes.
a. 22 pairs of autosomes
b. 01 pair of sex chromosomes
KARYOTYPE
 A method of organizing the chromosomes
of a cell in relation to number, size, and
type.
HOMOLOGOUS CHROMOSOMES
 Are paired chromosomes with genes for the
same trait arranged in the same order.
(Ex. Eye color, hair color , height, one may
code for blue , blonde, tall, its homolog may code
for brown , blonde short)
 Homologous chromosomes may have
different alleles on them
 ALLELE (gene form for each variation of a
trait of an organism)
 ZYGOTE (Fertilized egg which has a diploid
number of chromosomes)
Humans have 23 Sets of Homologous
Chromosomes
Each Homologous set is made up of 2
Homologues.
AUTOSOMES
(The Autosomes code for most of the
offspring’s traits)
In Humans the “Autosomes” are sets 1-22
SEX CHROMOSOMES
 The Sex Chromosomes code for the sex of
the offspring.
 XX FEMALE; XY MALE
 In Humans “Sex Chromosomes” are the 23rd
set
PROPHASE I: PACHYTENE or
PACHYNEMA
 synapsis is complete.
 The two homologous of each bivalent
appears to be attached with each other at
one or more points , these attachments are
known as chiasmata .
 Characterized by a fully forms
synaptonemal complex
 Crossing over is a precise breakage,
swapping and reunion between two non-
sister chromatids.
 Crossovers make new gene combinations
and which are an important source of
genetic variations in populations.
 Crossing Over
Tetrads are so tight that non-sister chromatids
from the homologous pair actually exchange
genetic material.
 Crossing over (variation) may occur
between non-sister chromatids at the
chiasmata (exchange of genetic material).
 Crossing over: segments of non-sister
chromatids break and reattach to the other
chromatid.
 Chiasmata (chiasma) are the sites of
crossing over.
 Results in a new combination of alleles
ANOTHER WAY MEIOSIS MAKES LOTS OF
DIFFERENT SEX CELLS-CROSSING-OVER
CROSSING OVER MULTIPLIES THE
ALREADY HUGE NUMBER OF DIFFERENT
GAMETE TYPES PRODUCED BY
INDEPENDENT ASSORTMENT.
 During 1st division, homologous
chromosomes exchange genes during
process called “crossing over”
 These homologous chromosomes separate
during 2nd division of meiosis—so
chromosomes in gametes are different
from each other due to crossing over
 Crossing over increases genetic variation
NO CROSSING OVER
-Daughter cells are identical to parent cells
CROSSING OVER
-Causes genetic variation
(Daughter cells are NOT identical to parent cell)
CROSSING OVER
 Homologues break identical locations ,then
rejoin opposite partners.
 New combinations of the alleles on each
chromosome.
 Occurs randomly several times on every
chromosome.
 Result in mixing of the genes you inherited
from your parents.
PROPHASE I: DIPLOTENE or DIPLONEMA
 DNA recombination is complete.
 The chromatids continue to shorten and
thicken and the four sister chromatids in
a group is called a tetrad.
 The synaptonemal complex begins to
breakdown.
 The paired chromatids begin to pull
apart
 The chiasmata tend to become
terminalized as the meiotic prophase
continues.
PROPHASE I :DIAKINESIS
 The chromosomes become shorter and
thicker due to condensation.
 Nucleolus and nuclear envelope disappear
 The spindle apparatus becomes organized
 The centrioles migrate away from one
another.
METAPHASE
 Shortest phase
 Tetrads (bivalents) align on the
metaphase plate.
 Homologous chromosomes line up
together in pairs.
 One homologue is pulled above the
metaphase plate, the other below
 The centromere of homologous
chromosomes of each bivalent stretch
out on either side
METAPHASE I
 INDEPENDENT ASSORTMENT OCCURS:
1. Orientation of homologous pair to poles is
random
2. Variation
3. Formula:2n
Example: 2n=4
Then n=2
Thus 2^2=4 combinations
VARIATION FROM GENETIC
RECOMBINATION
 Independent assortment of
chromosomes
 meiosis introduces genetic variation
 gametes of offspring do not have
same combination of genes as
gametes from parents
 Random assortment in humans produces
2^23 (8,388,608) different combinations in
gametes
ANAPHASE I
 Homologous chromosomes separate and
move towards the poles.
 Spindle fibers attach to the centromeres of
each pair.
 Centromeres DO NOT split like the do in
mitosis
 Sister chromatids remain attached at their
centromeres.
 Now each cell will get one chromosomes
from each homologous pair.
During Anaphase I, original chromosomes
separate, so reduction in the number of
chromosomes from 2n to n number, yet the sister
chromatids remain together
TELOPHASE I
 Each pole now has haploid of METAPHASE II
chromosomes.  Chromosomes line up on the
 Spindle fibers breakdown metaphase
 Chromosomes uncoil , nuclear envelope
organized around two groups of ANAPHASE II
chromosomes , nucleolus reappears
 Centromeres split
 Cytoplasm divides
 Sister Chromatids Separate and
 Another cell division is needed because
the number of chromosomes has not move to opposite sides of the cell
been reduced
 After telophase I there maybe a shirt TELOPHASE II
interphase, but not always. It is  Nuclei form, spindle fibers
important to note that if a cell does have disappear
a second interphase , there is No  Cytokinesis occurs
replication of chromosomes  The number of chromosomes in
 Cytokinesis occurs and two haploid each daughter cell has now been
daughter cells are formed. reduce by half
REMEMBER: 4 haploid daughter
Cytokinesis involves the information of a cleavage
furrow, resulting in the pocketing of the cell into two
cells produced; gametes = sperm or
cells. At the end of telophase I and Cytokinesis, egg
two daughter cells are produced, each with one half
of the number of chromosomes (haploid set of
replicated chromosomes) of the original parent cell.

RECAP:
VARIATION
 Important as the raw material for NATURAL
MEIOSIS II SELECTION
 No Interphase II  CROSSING OVER (prophase I)
(or very short – no more DNA replication)  INDEPENDENT ASSORTMENT
(metaphase I)
 Remember: Meiosis II is similar to mitosis  RANDOM FERTILIZATION
but remember the chromosomes did not
duplicate FUNCTIONS OF MEIOSIS
 Consists of: 1. Production of haploid (n) gametes
 Prophase II 2. Production of genetic variation
 Metaphase II 3. Segregation of two alleles of each gene
 Anaphase II
4. Recombination between linked genes
 Telophase II
5. Facilitates segregation and independent
assortment of chromosomes and genes
PROPHASE II
6. Essential for continuity of generation
 Chromosomes begin to line up in the
middle of the cell.
 Spindle Fibers begin to form
FURTHER INFORMATIONS:
 CHROMOSAL ANOMALIES Normal 1st & 2nd meiotic division & Two types of
 Teratology non-disjunction
 Causes of congenital malformations:
a) Genetic factors (chromosomal
abnormalities)
 Numerical
 Structural
b) Environmental Factors (drugs,
viruses etc.)

TRISOMIES OF CHROMOSOMES
 Presence of 3 copies of a chromosome
 Trisomy of Autosomes (13,18,21)
 Trisomy of sex chromosomes (xxx, xxy, xyy)

TRISOMY OF AUTOSOMES
a) TRISOMY 13 or D-trisomy (PATAU
SYNDROME)
NUMERICAL CHROMOSOMAL  1st describe by Bartholin (1657) and
ABNORMALITIES redefine by Patau (1960)
 Changes in the number of chromosomes:  Chromosomal Complement: 47, (XX
 POLYPLOIDY (Somatic cells contain or XY), +13
multiple haploids)  Phenotype; M or F
3n, 4n, 5n, etc.  Incidence: 1;12,000
 ANEUPLOIDY (heteroploidy) FEATURES:
(Deviation from the diploid number  Bilateral cleft lip/palate
of chromosomes)  Rocker-bottom heel
2n + 1, 2n – 1 etc.  Sloping Forehead
 Malformed Ears
MECHANISM OF POLYPLOIDY  Microphthalmia
a) Failure of pulling apart of 2 chromatids
b) Reduplication of Chromosomes w/o b) TRISOMY 18 or E-trisomy
dissolving nuclear membrane (EDWARDS SYNDROME)
c) Failure of cytoplasmic division
 Chromosomal Complement: 47, (XX
or XY), +18
TYPES OF POLYPLOIDY
 Phenotype; M or F
1. Autoploidy; even-numbered
 Incidence: 1;8,000
multiples of haploid
FEATURES:
a) Tetraploidy (92)
b) Hexaploidy (138)  Webbing of neck
c) Octaploidy (184)  Short sternum
2. Allopolyploidy; odd-numbered  Clenched fist with
multiples of haploid chromosomes overlapping or fingers
a) Triploidy (69)  Hypoplastic Nails
b) Pentaploidy (115)  Growth Retardation
c) Heptaploidy (161)
c) TRISOMY 21 or G-trisomy (DOWN
MECHANISM OF ANEUPLOIDY SYNDROME)
 NON-DYSJUNCTION: failure of separation  Chromosomal Complement: 47, (XX
of chromosomes during cell division. or XY), +21
 Formation of 2 types of gametes (both  Phenotype; M or F
abnormal)  Incidence: 1;8,000
 Fusion of normal and abnormal gametes
can result to TRISOMY or MONOSOMY
 May involve autosomes or sex
chromosomes
 FEATURES:
 Severe mental deficiency
with decline in the IG with
age
 Brushfield spots in iris
 Simian crease
 Scrotal tongue
 Clinodactyly of 5th digit

TRISOMY OF SEX CHROMOSOMES

a) TRISOMY X or TRIPLE X SYNDROME
 47, XXX
 1:1000 (Female)
 Don’t have much symptoms or only
have mild symptoms
SIGNS AND SYMPTOMS:
 Flat Feet
 Seizures
 Psychological problems
 Epicanthal Folds in eyes
 Hypotonia (Weak muscle
tone)
b) XXY or KLINEFELTER SYNDROME
 47, XXY
 Men who are born with extra X
chromosome
FEATURES:
 Breast development
 Wide hips
 Narrow Shoulders
 Fewer chest hairs
 Female-type pubic hair
pattern

c) XYY SYNDROME
 47, XYY
 Men who are born with extra Y
chromosome
SIGNS AND SYMPTOMS:
(BABY)
 Hypotonia
 Delayed motor skill
 Difficulty in speech
(YOUNG CHILD/TEENAGER)
 Autism
 Hypotonia
 Learning disabilities

d) X or TURNER SYNDROME
 Missing an X chromosome on 23rd
pair
SIGNS AND SYMPTOMS:
 Short stature
 Brown Spots
 No menstruation
 Rudimentary ovaries
Gonadal Streak
 Widely Spaced Nipples
REGULATION OF CELL DIVISION 3 MAJOR CHECKPOINTS:

COORDINATION OF CELL DIVISION

 Multicellular organism needs to coordinate
cell division across different tissues and
organs
 Critical for normal growth,
development and maintenance
o Coordinate timing of cell
division
o Rate of cell division
o Not all cells have the same
cycle  G1/S CHECKPOINT
 Critical
FREQUENCY OF CELL DIVISION  Primary decision point (restriction point)
 Varies by cell type  If cell receives “GO” signal, it divides
 Embryo (Cell cycle < 20 min) (internal signal: cell growth (size), cell
 Skin cells (divide through out life; 12- nutrition)
24 hrs cycle)  If cell does not receive signal, it exits cycle
 Liver Cells (retain ability to divide bu and switches to G0 phase (non-dividing,
researve; divides once every year or working state)
2)
 Mature nerve cells and Muscle cells  G0 PHASE
(do not divide after maturity;
 Non-dividing, differentiated state
permanently in G0)
 Liver cells (can be called back to cell cycle
OVERVIEW OF CELL CYCLE CONTROL by external cues)
 Nerve and muscle cells (highly specialized;
can never divide)
 Two irreversible points in cell cycle
 Replication of genetic material
ACTIVATION OF CELL DIVISION
 Separation of sister chromatids
 CELL COMMUNICATION SIGNALS
 CHECKPOINTS
 Chemical signals in cytoplasm gives cue
 Assessed and possibly halted
CENTOMERE  Signal means PROTEIN (activators;
o Point of attachment of between sister inhibitors)
chromatid. Kinetochore can be found. 
“GO-AHEAD” SIGNALS
KINETOCHORE  PROTEIN SIGNALS THAT PROMOTE
o Structure where spindle fibers attach CELL GROWTH & DIVISION
during cell division  internal signals (promoting factors)
 external signals (growth factors)
CHECKPOINT CONTROL SYSTEM
 PRIMARY MECHANISM OF CONTROL
 CHECKPOINTS  phosphorylation
 Cell cycle controlled by STOP and GO
o kinase enzymes
chemical signals at critical points
o either activates or inactivates cell
 Signal indicates if key cellular processes
have been completed correctly signals

CELL CYCLE SIGNALS

 Cell cycle controls
o CYCLINS
 Regulatory proteins
 Levels cycle in the cell

o CDK’S
 cyclin-dependent kinases
 phosphorylates cellular proteins
(activates or inactivates proteins)
 o CDK-CYCLIN COMPLEX
 Triggers passage through
different stages of cell cycle
CYCLINS AND CDKS
 Interaction of CDK’s and different cycline
triggers the stage of the cell cycle
CYCLINE AND CYCLIN-DEPENDENT
KINASES
 CDKS and cyclin drive cell from one phase
to next in cell cycle
 Genes for these regulatory proteins
have been highly conserved through
evolution
 Genes are basically the same in yeast,
insects, plants and animals
GROWTH FACTORS AND CANCER
 Creates cancer
o PROTO-ONCOGENES
 Normal growth factor genes that
become oncogenes (cancer-causing)
when mutated
 Stimulates cell growth
 If its ON can cause cancer
o TUMOR-SUPRESSOR GENES
 Inhibits cell division
 If switched OFF can cause cancer
 MUTATIONS IN CELL CAN BE
TRIGGERED BY:
 UV radiation; Chemical exposure;
Radiation exposure
 Heat
 Pollution; Cigarette smoke
 Age; Genetics
TRADITIONAL TREATMENTS FOR
CANCERS
 Treatments target rapidly dividing cells
 High-energy radiation (kills dividing
cells)
 Chemotherapy (Stops all process in
cells)
NEW “MIRACLE DRUG” (target protein found in
cancer cells)
 GLEEVEC (treatment for adult leukemia
and stomach cancer (GIST))