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A-Level Biology Tuition Singapore/H2 Biology Tuition/JC Biology Tutor
TOPIC 3: GENETICS OF VIRUSES AND BACTERIA – Part 1
LEARNING OUTCOME
(a)Discuss whether viruses are living or non-living organisms and explain why viruses are obligate parasites.
ESSAY ANSWER
Arguments for Viruses being living
Arguments for Viruses being non-living
Possess genes/genetic material (DNA or RNA)
Have no cellular structure
Capable of reproducing by producing multiple copies of themselves
Cannot reproduce or carry out metabolic activities outside of a host
cell (e.g. ATP synthesis) and have no cellular machinery
Evolve by natural selection
Reproduce by assembly, not cell division
Why obligate?
Reproduce only within a host cell.
Contain only one type of nucleic acid (either DNA or RNA – which can be
single-stranded or double-stranded, but NOT both).
All viruses are parasitic.
Can infect and parasitize only a limited range of host cells.
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TOPIC 3: GENETICS OF VIRUSES AND BACTERIA – Part 2
LEARNING OUTCOME
(b)Describe the structural components of viruses.
ESSAY ANSWER
Main structural components of viruses:
Core – the genetic material, either DNA or RNA. (i.e. single-stranded OR
double-stranded)
Capsid – a protective coat of protein surrounding the core.
Capsids can come in many forms (helical (tobacco mosaic virus),
icosahedral (adenoviruses) and complex (bacteriophage T4).
Capsomeres – capsids are often built up through self-assembly of identical
repeating subunits
Nucleocapsid –core and capsid.
Envelope –additional lipoprotein layer around the capsid derived from the cell
surface membrane of the host cell.
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TOPIC 3: GENETICS OF VIRUSES AND BACTERIA – Part 3
LEARNING OUTCOME
(c)Describe the reproductive cycles of the following virus types:
i. bacteriophages that reproduce via a lytic cycle, e.g. T4 phage;
ESSAY ANSWER
T4 bacteriophage:
Adsorption – attachment of T4 phages onto specific receptor sites on surface
of host
– specific receptor sites: cell wall lipopolysaccharides or proteins
– attachment: via tail fibres
Penetration – Injection of phage DNA
– baseplate is firmly attached on the host cell surface
- tail sheath contracts and tail tube penetrates the outer membrane
– phage enzyme (lysozyme) “drills” a hole in the bacterial wall
– viral DNA is injected through the bacterial cell wall
- phage DNA enters bacteria cytosol
Replication – Replication of phage DNA & Synthesis of phage proteins
– Phage genome is expressed, using the RNA polymerase and ribosomes from its host cells.
- Phage proteins, including enzymes, encoded by the phage genome,
are produced.
- Enzyme degrade bacterium host DNA, shutting down thebacterium’s gene expression and its macromolecular synthesis (protein, RNA and DNA).
- Replication of phage DNA occurs using the bacterium’s metabolic
machinery, e.g DNA polymerase
- Transcription of phage DNA.
- Synthesis of phage proteins, enzymes and structural components
using bacterium’s metabolic machinery, e.g. ribosomes
Assembly – spontaneous assembly of viral particles
– Spontaneous assembly
Release – causing lysis of bacterium host cell
- Phage-encoded lysozyme breaks down the bacterial peptidoglycan
- osmotic lysis and release of the intact new bacteriophages,
- host cell lysis
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JC1 Promo Exams and JC2 Prelim Exams Preparatory Classes
for Biology.
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Question
(a) Explain how named factor(s) may increase the chance of cancerous growth [5 marks]
(b) Therapeutic genes can be introduced into stem cells. Discuss why the genes used are more likely to be obtained from a cDNA library, than a genomic DNA library.[5 marks]
Ans
(A)
1. Source: Chemical carcinogens like tar from cigarettes/ionising radiation from UV rays or X-ray/viruses like the human papillomavirus/Epstein barr virus (reject “diet” or “smoking”)
2. Mutations in DNA take place in the form of change in sequence of bases/base substitution/deletion/insertion/inversion.
3. Mutations can also convert proto-oncogenes such as the Ras to oncogenes
4. When proto-oncogenes are converted to oncogenes, it is a gain of function mutation,
5. Resulting in (i) increased protein activity / (ii) increased protein quantity / (iii) active promoter / upregulation of gene expression
6. Carcinogens can also cause the mutation of the tumour suppressor genes such as the p53 gene.
7. This leads to the loss of function mutation.
8. Resulting in inability to control cell cycle / DNA repair / apoptosis / OWTTE
9. With the accumulations of mutations, this leads to excessive cell division/proliferation/lack of programmed cell death or apoptosis.
(b)
1. Genes obtained from the cDNA library lack introns, whereas genes obtained from genomic DNA library still possess introns.
2. Therefore, genes that are obtained from cDNA library can bypass the need for post-transcriptional modifications.
3. Genes obtained from the cDNA library can be genetically-engineered to be placed directly after a constitutive promoter to ensure its continual expression in target cells.
4. Genes obtained from the genomic DNA library may contain an existing promoter that is either weak or not active in the target cells.
5. Sometimes, alternative splicing of genes may derive gene product which is different from the desired gene product, using genes from the cDNA library will ensure the correct gene product is utilised.
6. Genes from cDNA library will be shorter in length as compared to genes from the genomic DNA library due to the absence of introns.
7. A shorter DNA length will ensure facilitate ease of packaging into vectors such as viruses or liposomes.
8. function and sequence of cDNA are known
9. in cDNA specific genes are obtained
10. easier to find the gene sequence with cDNA
REJECT: any view point from Genomic Library perspective.
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DNA and Genomics Mutation Cancer
Important concepts
1. DNA and Genomics
· DNA replication process (leading and lagging strand synthesis), end replication problem, Meselson-Stahl experiment (proves semi-conservative replication)
· Gene expression
· Genetic code
· Transcription, amino acid activation, translation
· Roles of various enzymes, ribosomes, mRNA, tRNA, rRNA in these processes
· How structure is related to function – ribosomes, mRNA, tRNA, rRNA, DNA
· Comparisons between processes
· Replication vs transcription
· Transcription vs translation
· Replication vs translation
· Replication vs reverse transcription
2. Mutation
· Types of mutation
· Effect on DNA -* mRNA -* protein STRUCTURE -* protein PROPERTY -* protein FUNCTION -* effect on PHENOTYPE
3. Cancer
· Molecular level – oncogenes , tumour suppressor gene
· Cellular level – loss of control of cell cycle checkpoint
· Possible modes of treatment
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