Table of contents
- 1. Introduction to Genetics51m
- 2. Mendel's Laws of Inheritance3h 37m
- 3. Extensions to Mendelian Inheritance2h 41m
- 4. Genetic Mapping and Linkage2h 28m
- 5. Genetics of Bacteria and Viruses1h 21m
- 6. Chromosomal Variation1h 48m
- 7. DNA and Chromosome Structure56m
- 8. DNA Replication1h 10m
- 9. Mitosis and Meiosis1h 34m
- 10. Transcription1h 0m
- 11. Translation58m
- 12. Gene Regulation in Prokaryotes1h 19m
- 13. Gene Regulation in Eukaryotes44m
- 14. Genetic Control of Development44m
- 15. Genomes and Genomics1h 50m
- 16. Transposable Elements47m
- 17. Mutation, Repair, and Recombination1h 6m
- 18. Molecular Genetic Tools19m
- 19. Cancer Genetics29m
- 20. Quantitative Genetics1h 26m
- 21. Population Genetics50m
- 22. Evolutionary Genetics29m
17. Mutation, Repair, and Recombination
DNA Repair
Problem 18
Textbook Question
It has been shown that infectious agents such as viruses often exert a dramatic effect on their host cell's genome architecture. In many cases, viruses induce methylation of host DNA sequences in order to enhance their infectivity. What specific host gene functions would you consider as strong candidates for such methylation by infecting viruses?

1
Understand the context: Viruses can manipulate the host genome to enhance their infectivity. DNA methylation is a common epigenetic modification that silences gene expression. Consider which host genes, if silenced, would benefit the virus.
Identify host genes involved in immune response: Genes that regulate the host's antiviral defense mechanisms, such as interferon-stimulated genes (ISGs), are strong candidates for methylation. Silencing these genes would weaken the host's ability to fight the infection.
Consider genes involved in apoptosis: Apoptosis, or programmed cell death, is a defense mechanism that prevents viral replication. Viruses may methylate genes that promote apoptosis, such as *TP53* (p53), to keep the host cell alive and allow viral replication.
Evaluate genes regulating cell cycle control: Viruses often hijack the host's cell cycle machinery to promote their replication. Methylation of tumor suppressor genes like *RB1* (retinoblastoma protein) or *CDKN2A* (p16) could disrupt cell cycle checkpoints, favoring viral replication.
Think about genes involved in DNA repair: Methylation of DNA repair genes, such as *BRCA1* or *MLH1*, could increase genomic instability, which might benefit the virus by creating a more permissive environment for its replication and integration into the host genome.

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Key Concepts
Here are the essential concepts you must grasp in order to answer the question correctly.
DNA Methylation
DNA methylation is a biochemical process involving the addition of a methyl group to the DNA molecule, typically at cytosine bases. This modification can regulate gene expression by silencing genes, thereby influencing various cellular functions. In the context of viral infections, viruses may exploit this mechanism to alter host gene expression, enhancing their own infectivity.
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Host Gene Functions
Host gene functions refer to the roles played by genes within the host organism that are crucial for maintaining cellular processes, such as immune response, cell cycle regulation, and apoptosis. Viruses may target specific host genes that are involved in these processes to evade immune detection or promote viral replication, making them prime candidates for methylation.
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Viral Manipulation of Host Genomes
Viral manipulation of host genomes involves strategies employed by viruses to alter the genetic and epigenetic landscape of their host cells. This can include the induction of methylation changes that suppress host defenses or promote a favorable environment for viral replication. Understanding these interactions is essential for identifying which host genes are likely to be affected during viral infections.
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Related Practice
Textbook Question
DNA damage brought on by a variety of natural and artificial agents elicits a wide variety of cellular responses involving numerous signaling pathways. In addition to the activation of DNA repair mechanisms, there can be activation of pathways leading to apoptosis (programmed cell death) and cell-cycle arrest. Why would apoptosis and cell-cycle arrest often be part of a cellular response to DNA damage?
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