1) Telomeres: why do they shorten? And how does the cell make them longer?

2) (i) describe prokaryote protein formation process

(ii) how do eukaryotes make hnRNA? List the things that must be done for
hnRNA to become mature mRNA.
3) What is RNA interference? Briefly describe how siRNA works.
4) (i) describe the differences between qualitative
and quantitative genetics
(ii) why do some anomalies which should be multifactorial in inheritance
display differences in occurrence in different sexes?
5) What is antigen shift in influenza virus and how does it come about?
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1.
Telomeres are highly repetive sequences found at the end of chromosomes.
During DNA replication, RNA primers are located at the ends of DNA strand
(and several primers are present in the lagging strand).
When the RNA primers are substituted by DNA, via nick translation, a problem
arises since there is no DNA upstream from the first RNA primer, and so this
primer cannot be replaced. This results in chromosome shortening.
Telomeres are made longer by the enzyme Telomerase. Telomerase adds the
same, repetitive, 6 nucleotide sequence to the end of the telomeres so as to
keep on elongating them.
2.
(i)
Prokaryotic protein synthesis starts with mature mRNA formed by the
transcription of DNA to pre-mRNA, and post-transcriptional modification of
the pre-mRNA into mRNA if applicable.
Two, irreguarly shaped, ribosomal sub units (one large, one small) join
to form the P, A and E sites, and the groove for the mRNA.
As the mRNA is read in codons (3-set of nucleotides), corresponding tRNA,
containing the suitable anti-codon enter the first site, the A site, and
cause their attach amino acid to add onto the forming polypeptide chain.
The empty tRNA exits the ribosome from the E site; the polypeptide chain is
on the P site and new tRNA enters from the A site.
Release factors cause the the polypeptide chain is released,
post translational modification and folding, usually with the help of
chaperones like heat schock protein (HSP) 70 and 60 occurs, to form the
final protein product.
(ii)
hnRNA, or pre-mRNA is the raw product of transcription.
Transcription is the process whereby a parental DNA strand acts as a
template for the formation of the pre-mRNA.
The process involves ADD REST TONIGHT.
3.
RNA interference is a type of RNA modification therapy, other types being
the use of antisense oligonucleotides and the use of ribozymes.
It is useful as it disrupts RNA which is responsible for a wide range of
diseases, including HIV.
RNA makes use of siRNA, or short interference RNA, which is a short piece
of double stranded RNA which is capable of entering the cell and disrupt
the process of mRNA translation and also causes mRNA degradation.
siRNA interference works in the following manner:
The double-standed RNA (dsRNA) enters the cell via a medium, such as a
lipoprotein or exosome.
The dsRNA is cleaved by the enzyme called dicer into anti-sense and sense
siRNA.
Sense siRNA is degraded and the antisense siRNA forms a protein complex
called RNA-Induced Silencing Complex (RISC).
The RISC then causes degradation of the mRNA present.
4.
(i)
Qualitative:
- Single gene inheritance
- Characters of kind
- Examples: Eye colour, Hair colour
- Discontinuous variation
- Environmental factors not important.
- Concerned with individual matings
Quantitative:
- Polygenic inheritance
- Characters of degree
- Examples: Height, weight
- Continuous variation
- Environmental factors very important
- Concerned with population matings
(ii)
This is not caused by sex chromosomes.
Rather, it is caused by the fact that sexes have different physiologies.
That is, the environmental factor differs (internal environment).
For example, in the case of height, males tend to be ~3cm taller than
females, even if the same genes are present and if they liver in the same
environment.
The difference in height is caused by the fact that males have more growth
hormone than females and so are naturally slightly taller.
When speaking of diesease, the same principle applies. Due to physiological
differences between males and females, it can be taken that the
distribution curves for genotypic liability to a condition are the same,
but the threshold differs, making one sex more likely to get a certain
condition than the other sex.
5.
In the Influenza virus, several types of antigens exist: H1, H2, H3, N1, N2.
Antigen shift is the process by which the antigens present on the surface
of the influenza virus rapidly shifts, for example from H1N1 to H3N2.
It occurs from a superinfection. This is when 2 virus strains are present
in the same animal. When this occurs, the 8 RNA genes which are incorporated
into the viroid seem to be random, therefore resulting in any mixture of
RNA genes between the two original viruses, causing a new virus to form
with a mixture of the two original viruses.
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2012 paper:
1.
The lagging strand is antiparallel to the leading stranding, and is in the
3' to 5' direction.
Since synthesis occurs in a 5' to 3' direction, this strand isn't
synthesized continuously like the leading strand.
Instead, the lagging strand is synthesized in fragments called Okazaki
fragments. An RNA primer is used to synthesize the first fragment, after
which another RNA primer is placed further downstream and synthesis occurs
until the first primer has been reached.
This repeats, forming numerous fragments.
The RNA primers are replaced by DNA, a process called nick translation
which occurs due to DNA Pol I, after which DNA Ligase joins the fragments
together to form the daughter strand.
2.
Steroid hormone - Steroid hormones may modify gene expression, either by
enhancing or repressing it. They are fat soluble and
work by binding to receptors, either on the cell surface
or in the cytoplasm, which then forms transcription
factors.
Promoter - Promoters are a short sequence of DNA that is present somewhere
on the same gene and increases transcription of the gene
towards its maximum potential.
DNA Methylation - DNA Methylation is involved in genomic imprinting.
What the methylation does is that is block the expression
of a particular gene.
Males and females methylate different genes, and this
genomic imprinting is involved in diseases such as
Prader-Willi syndrome and Angelman syndrome.
Chromatin remodelling - Chromatin remodelling is the change in the chromatin
from 'closed' to 'open', where 'open' chromatin
implies that the chromatin is more loosely wound
and can therefore participate in DNA synthesis or
transcription of RNA.
Alternate splicing - Alternate splicing is an important post-transcriptional
modification of pre-mRNA where introns are excised from
the gene. It is important because, apart from creating
a function gene, it also explains how one gene can
code for many proteins, as some exons may be excised in
some proteins but not in others.
3.
a) Mitochondrial DNA - The DNA within mitochondria. It is 16.6kb long.
It has several distinct characteristic, such as the
fact that it lacks introns, has a high rate of
mutation (due to ROS, lack of histones, inefficient
DNA repair mechanisms, no proof-reading, etc.)
and the fact that it shows maternal inheritance.

b) Recessive epistasis - Recessive epistasis is a type of interaction
between two genes, not located on the same locus,
meaning that the expression of one gene may be
dependent on the other gene.
In recessive epistasis, if the genotype of an
allele is aa, it may prevent the expression of
an allele Bb, or BB.
The 9:3:3:1 ratio is modified to 9:3:4.
c) Single nucleotide polymorphisms - SNPs are single nucleotides which show
polymorphism, that is, there is a
significant variation in a population
in that there are at least two differ-
ent variants.
SNPs are used as genetic markers for
certain diseases and for pharmacology
studies.
Other genetic markers include VNTRs
and RFLPs.
4.
Four mechanisms by which the normal products of proto-oncogenes can be
distrupted to rpoduce neoplastic transformation are:
1. Gene translocation
2. Gene amplification
3. Point mutations
4. Viral insertion