BIOLOGY ASSIGNMENT

2
0200100

STUDENT NAME:Noor mohammed

STUDENT ID:202310446
SEMESTER: SEMESTER I 2023 2024
Question and answer rubric scoring sheet – do not remove from your work
Student Name: Noor mohammad
Student ID: 202310446
Student Total Score:
Rubric Student % Sophisticated
Assignment Score
Position and exceptions
are clearly stated.
Introduction 20 Organization is completely
and clearly outlined and
implemented (2 – 3 pts)
Research 40 Highly relevant to the
argument, is presented
accurately and completely.
Theory is relevant,
accurately described and
all relevant components
are included (3 – 4 pts)
Conclusions 20 Conclusion is clearly stated
and connections to the
research and position are
clear and relevant (2 – 3
pts)
Writing 20 Paper is coherently
organized and the logic is
easy to flow. There are no
errors and terminology is
clearly defined. Writing is
clear, concise and
persuasive (1 – 2 pts)
Total Score 100%
No pictures or tables required
Competent
Position is clearly stated.
Organization of argument is
clear in parts or partially
described and most
implemented (1 – 2 pts)
Research is relevant and
mostly accurate and
complete. However, there
are some unclear
components or minor errors.
Theory is relevant, accurately
described by some
components are missing or
unclear (1 – 2 pts)
Conclusion is clearly stated
and connections to the
research and position are
mostly clear, some aspects
may not be connected or
minor errors in logic are
present (1 – 2 pts)
Paper is generally well
organized and most of the
argument. There are only a
few minor errors or terms
not clearly defined. Writing is
clear but lacks conciseness (1
– 2 pts)
Needs work
Position is vague. Organization of
argument is missing, vague or
inconsistent (0-1 pts)
Research selected is not relevant to
the argument or is vague and
incomplete. Theory is not relevant
or only relevant for some aspects, is
not clearly articulated and/or has
incorrect components (0-1 pts)
Conclusion is not clear and the
connections to the research are
incorrect or unclear or just a
repetition of the findings without
explanation (0-1 pts)
Paper is poorly organized and
difficult to read. It does not flow
logically from one to another. There
are several errors and terminology
is not or poorly defined. Writing
lacks clarity and conciseness (0-1
pts)
 1. Synthetic biology has multiple uses. It can be even used to improve the diagnosis of disease and
make new treatments. An important part of developing new drugs is making them with fewer
side effects. Side effects happen when a drug binds to different cells and protein in the body
even though only a small number of these binding sites are required for the drug’s disease or
infection-fighting property. Synthetic biology can be used to make treatments directed only
towards the site of disease, treating the disease itself without causing any negative effects.
Describe how biology could assist make treatments that only go to the site of disease and cause
no side effects (3 marks)

In healthcare, synthetic biology can be used to improve diagnosis of disease, and it can be used to make
new treatments. An important part of developing new pharmaceuticals is making medicines with fewer
side effects. Side effects or ‘off-target’ effects tend to occur if a drug binds to lots of different cells and
proteins in the body, despite only a small number of these binding sites being necessary for its disease
or infection-fighting property. Synthetic biology can be used to make treatments directed only towards
the site of disease, treating the disease itself without causing any negative effects.

Many pharmaceuticals are produced naturally by plants. These include pain relievers, morphine (an
opioid) from poppies, and salicylic acid (a plant hormone and precursor to aspirin) from willow bark but
producing a high yield of these compounds is not always easy. Synthetic biology can be used to engineer
yeast to produce medicines more efficiently and cheaply on a large scale. Artemisinin, a malaria
treatment, was the first drug produced in this manner. Artemisinin is naturally produced by sweet
wormwood, but the pharmaceutical company Sanofi has assembled the biosynthetic pathway that
produces the precursor of artemisinin, artemisinic acid, in Saccharomyces cerevisiae (S. cerevisiae,
baker's yeast). The yield of artemisinin was increased by re-engineering yeast cells to include the genes
required for the pathway. Metabolic engineering is the process of using genetic engineering to increase
or establish a cell's production of a substance.

It is remarkable that synthetic biology has been used to re-engineer the patient's own cells to fight
cancer. T lymphocytes (or T cells) from the patient are isolated and genetically modified to express a
chimeric antigen receptor (CAR). CAR is a fusion protein that contains an antibody that recognizes the
CD19 protein found on malignant B cells. The reintroduced modified 'CAR-T' cells are now capable of
recognizing cancer cells as malignant. CAR-T cells can then ensure that the immune system targets the
cancerous B cells for destruction. CAR-T cells can live in patients for years, if not decades, making them a
highly effective and targeted therapy for ALL.

To summarise, synthetic biology holds great promise in the field of healthcare by improving disease
diagnosis and enabling the development of targeted treatments with fewer side effects. The innovative
use of genetic engineering, such as re-engineering yeast for efficient drug production and modifying a
patient's own cells for cancer treatment, exemplifies synthetic biology's transformative potential in
advancing medical therapies. This approach not only improves treatment precision but also provides a
path to more cost-effective and scalable pharmaceutical production, as demonstrated by the successful
synthesis of Artemisinin for malaria treatment.
 2. MicroRNAs are short non-coding RNAs (~22-nucleotides in length) that bind to a complementary
mRNA and regulate gene expression at the post-transcriptional level. miRNAs are highly
expressed in the CNS including the brain and spinal cord.
Describe how microRNAs play an important role in the brain and spinal cord (3 marks)

The crucial post-transcriptional regulator of gene expression is microRNA. The central nervous system
contains a wide variety of microRNAs, which mediate the neurodevelopment of the brain and spinal
cord. The brain's altered levels of miRNA expression during development serve as biochemical cues for
reprogramming cell division, death, and fate selection. Micro-RNAs are small non-coding RNAs that are
essential for preserving synaptic plasticity and cell fate specification. These microRNAs are packaged
within vesicles called exosomes, which are produced in varying amounts following brain injury and are
crucial for facilitating their intercellular communication and passage through the blood-brain barrier.
Many miRNAs have been found to be potential regulators of hemostasis and CNS development.

They are widely expressed in the central nervous system (CNS), where they interact with their target to
either up- or down-regulate the expression of certain genes (like Bcl-2) or Src, for example. They are
involved in a number of important processes, such as apoptosis (miR-124 and miR-21), neuronal death,
and astrogliosis in the spinal cord. Molecular signaling linked to miRNAs affects the process of astrocyte
proliferation and astrogliosis. MiR-16, miR-15b, and miR-21 all influence several molecular pathways in
the process of apoptosis, such as the Bak, Bcl-2, and Bax pathways. Let-7, miR-15b, and miR-16 all
downregulate Bcl-2, an anti-apoptotic protein that also triggers the release of cytochrome c. miRNA also
promotes neuronal development and functional recovery in addition to regeneration.

MiRNAs maintain the balance between several cell division cycle genes and the brain neurotrophic
factor (BDNF) gene, which both influence self-repair following spinal cord injury. MiR-96 inhibits the
expression of transcription factors FOXO3a and FOXO1, which in turn controls cell proliferation,
migration, and cycle. Complex interactions and modifications occur at the cellular and protein levels as a
result of miRNA expression. Regulating the expression of microRNAs may help improve therapeutic and
clinical approaches to counteract the debilitating effects of brain and spinal cord injury.

In conclusion, microRNAs play an important role in the central nervous system by acting as post-
transcriptional regulators of gene expression. Their role in neurodevelopment, synaptic plasticity, and
cell fate specification highlights their importance in shaping the complex molecular processes that occur
within the brain and spinal cord. MicroRNAs' inclusion in exosomes, impact on apoptosis and astrocyte
proliferation, and ability to influence self-repair mechanisms after spinal cord injury highlight their
diverse functions. Understanding and manipulating microRNA expression has the potential to
significantly advance therapeutic strategies for dealing with the consequences of brain and spinal cord
injuries.
 3. Alzheimer’s disease is a neurodegenerative disease that progresses and has no cure. It causes
loss of memory and cognitive decline. Mitochondrial issues are found in brains of patients with
AD.
What role do mitochondria play in the brains of patients with Alzheimer’s disease and what
happens to the mitochondria in the brain cells of such individuals? (2 marks)

The "powerhouse" of a cell, mitochondria constantly produce ATP to maintain proper operation.
Protons are forced through the highly selective and low-permeable inner membrane of the
mitochondria by a strong electrochemical force required for the continuous oxidative phosphorylation
process, which produces ATP. In addition to their usual function of producing ATP, mitochondria are also
involved in calcium signaling, the production of reactive oxygen species (ROS), stress responses, and the
control of pathways leading to cell death. Numerous pathological conditions, including ageing, cancer,
diabetes, neurodegenerative diseases, and cardiovascular disorders, are caused by deficiencies in these
functions.

When Ca2+ levels in mitochondria are not controlled, they can become toxic and trigger a chain of
events that ultimately results in cell death. The study revealed a decrease in the activities of enzymes
involved in mitochondrial energy production in AD brains. These enzymes include pyruvate
dehydrogenase complex, mitochondrial isocitrate dehydrogenase, complex IV cytochrome c oxidase
(COX), α-ketoglutarate dehydrogenase (αKGDH), and ATP synthase complex. Since mitochondria
regulate both the pathways leading to cell death and energy metabolism, they are ideally positioned to
play a critical role in the survival or demise of neuronal cells. A substantial body of research indicates
that oxidative damage and mitochondrial dysfunction play a part in the etiology of Alzheimer's disease.

Understanding mitochondria is crucial to comprehending how cells function. The loss of neuronal
synaptic density and synapse number, along with a build-up of aberrantly folded protein peptides in the
brain, are characteristics that categorize Alzheimer's disease. These proteins are the source of amyloid
plaques and neurofibrillary tangles, two distinct forms of Alzheimer's pathology. In order to cause
metabolic dysfunction and interfere with the mitochondria's role in the pathophysiology of Alzheimer's
disease, AB-peptides preferentially accumulate within the mitochondria prior to plaque formation. The
patient's memory and learning will be negatively impacted by the protein peptides as the disease
progresses. resulting in the eventual death of brain cells.

In conclusion , mitochondria, the cellular powerhouses, play an important role in energy production,
calcium signaling, and cell survival. Dysregulation of mitochondrial functions has been linked to a
number of pathological conditions, including Alzheimer's. The investigation of mitochondrial
involvement in diseases such as Alzheimer's emphasizes the significance of understanding their dual role
in energy metabolism and cell death pathways. The buildup of AB-peptides within mitochondria
contributes to metabolic dysfunction and, as a result, the progression of Alzheimer's disease, which
leads to cognitive decline and neuronal death. Understanding mitochondria is critical for unravelling the
complexities of cellular function and advancing therapeutic approaches for mitochondrial dysfunction-
related conditions.
 4. Aurora kinases are essential for cell division and are primarily active during mitosis. Describe the
role that these play in mitosis? (2 marks)

As members of the serine/threonine kinase family, aurora kinases are crucial for the regulation of the
cell cycle. They were initially found in Drosophila. Monopolar spindles are formed when mutations in
these proteins prevent the centrosome from splitting. Three Aurora kinases are found in mammals:
Aurora-A, Aurora-B, and Aurora-C.
In mitosis, Aurora-A and Aurora-B are indispensable. While Aurora-B is involved in chromatin
modification, microtubule-kinetochore attachment, spindle checkpoint, and cytokinesis, Aurora-A is
primarily involved in centrosome function, mitotic entry, and spindle assembly.
Aurora-A localises to pericentriolar material during the G2 phase, which is necessary for centrosome
maturation. The centrosomal protein, which has the ability to bind γ-tubulin and other centrosomal
components, needs Aurora-A to be localised. Following nuclear envelope breakdown, Aurora A also
localises to the pole-proximal ends of microtubules, where it plays a role in spindle assembly.

Centrosome separation is another function of Aurora-A. At the G2-M transition, duplicate centriole pairs
split off and march to the cell's opposite poles to properly form a bipolar spindle. There is proof that
functional Aurora-A is necessary for centrosome separation.
In addition to centrosome separation and spindle assembly, Aurora-A aids in the G2 to M phase
transition. Aurora-B controls the modification of chromatin proteins. It has been discovered that during
mitosis, Aurora-B phosphorylates histone H3 at Ser10, Ser28, and its variant CENP-A at Ser7.
To ensure precise chromatid separation, every kinetochore must be attached to microtubules originating
from the opposing poles. Two mechanisms are activated in cells to control this process: the spindle
checkpoint and the correction of error attachment. It has long been hypothesised that Aurora-B is
essential to both pathways because inhibition of Aurora-B increases the frequency of syntenic and/or
merotelic attachments in prometaphase cells and causes these cells to enter anaphase without arrest
and with misaligned chromosomes.
Furthermore, it has been discovered that during mitotic spindle assembly, centromeric MCAK is
phosphorylated by Aurora-B, which inhibits its ability to depolymerize microtubules. To maintain the
kinetochore microtubules in a more stable form during mitosis, Aurora-B can phosphorylate MCAK if
microtubule-kinetochore attachment is bipolar. If not, Aurora-B stops phosphorylating MCAK, and the
kinetochore microtubules depolymerize so that other microtubules can grab the detached kinetochore.
It is possible that Aurora-B and protein phosphatase control the kinetochore-microtubule connection
through the dynamics of phosphorylation and dephosphorylation modification of the MCAK protein.
An important part of cytokinesis is played by Aurora-B. Polyploidy results from the depletion of Aurora-
B, which causes cytokinesis failure in Drosophila S2 cells and C. elegans embryos.

In conclusion, Aurora kinases are key regulators of the cell cycle, with Aurora-A and Aurora-B playing
essential roles in mitosis. Aurora-A influences centrosome function and spindle assembly, while Aurora-
B is crucial for chromatin modification, microtubule-kinetochore attachment, and cytokinesis.
Dysregulation of these kinases can lead to cellular abnormalities, highlighting their importance in
maintaining genomic stability. Understanding their functions provides valuable insights for potential
therapeutic interventions in conditions associated with cell cycle dysregulation.
References
Garner, K. L. (2021 Nov). Principles of synthetic biology.

Lawrence D. Longo, M. C. (march 6 ,2019). MicroRNAs in brain development and cerebrovascular

pathophysiology.

Department of Pharmacology & Toxicology and Higuchi Biosciences Center, S. o. (2014 Dec 31). From a
Cell’s Viewpoint: Targeting Mitochondria in Alzheimer’s disease.

Seyed Khalil Rashidi1 Ata Kalirad2 Shahram Rafie3, 4. E. (4 sep 2023). The role of microRNAs in
neurobiology and pathophysiology of the hippocampus.

Paula I. Moreira, C. C. (21 October 2009.). Mitochondrial dysfunction is a trigger of Alzheimer's disease
pathophysiology.

Paulina Bastian, 1. J.-J.-P. (Feb 2021). Regulation of Mitochondrial Dynamics in Parkinson’s Disease—Is 2-
Methoxyestradiol a Missing Piece?

Laboratory of Nervous System Diseases and Therapy, G.-N. U. (2018 Sep 19). The functional diversity of
Aurora kinases: a comprehensive review.