| Programme | SoLS - Life Sciences Modules Database (Level 3) CC47 - B.Sc. Hons. Biochemistry and Genetics (Part 2 - Restricted Group 1) CC4R - M.Sci. Hons. Biochemistry and Genetics (Part 2 - Restricted Group 1) |
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| Year | ![]() Select a new weight:
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| Accrediting Bodies | |
| Module Code | LIFE3002 |
| Credits | 10 |
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Total Credits:
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10.00
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Level:
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3
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Target Students:
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Honours Biology, Biochemistry, Genetics, Zoology and Microbiology. Available to JYA/Erasmus students.
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Summary Of Content:
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Why do we age and succumb to cancer? Has human civilization exposed a process of cellular decay for which evolution never prepared us? The age-related onset of cancer provides a stark reminder that we cannot avoid damage to the genetic blueprint on which life depends, and suggests that ageing may be a consequence of cellular activities that limit DNA damage and malignant transformation. To avoid the ravages of age on the 'disposable soma', the germline is refreshed each generation by means of reproduction. Sexual reproduction is underpinned by recombination, which shuffles the genome and ensures correct chromosome segregation in meiosis. The molecular mechanisms of recombination are conserved in bacteria, yeast and higher eukaryotes, and defects in recombination are linked to cancer pre-disposition and/or premature ageing in humans. This module examines how studies in bacterial and yeast model systems have uncovered the relationship between the somatic ageing observed during a single lifespan, and the necessity to maintain the genome intact from one generation to the next. This is despite our continuous exposure to mutagens and carcinogens of both natural and human origin. We will focus on the nature and consequences of genotoxic damage, and learn how microbiology, including model organisms such as Escherichia coli and Saccharomyces cerevisiae, has informed us about the mechanisms that avoid, repair or tolerate such damage. |
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Course Web Links:
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Why do we age and succumb to cancer? Has human civilization exposed a process of cellular decay for which evolution never prepared us? The age-related onset of cancer provides a stark reminder that we cannot avoid damage to the genetic blueprint on which life depends. Aging may be a consequence of cellular activities that limit DNA damage and malignant transformation.To avoid the ravages of age on the 'disposable soma', the germline is refreshed each generation by means of reproduction. Sexual reproduction is underpinned by recombination, which shuffles the genome and ensures correct chromosome segregation in meiosis. The molecular mechanisms of recombination are conserved in bacteria and eukaryotes, and defects in recombination are linked to cancer pre-disposition and/or premature ageing in humans.This module examines the relationship between the somatic ageing observed during a single lifespan, and the necessity to maintain the genome intact from one generation to the next. This is despite our continuous exposure to mutagens and carcinogens of both natural and human origin. We will focus on the nature and consequences of genotoxic damage and on the mechanisms that avoid, repair or tolerate such damage. |
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Education Aims:
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Offering School:
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Life Sciences
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Convenor:
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Requisites:
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N/A
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Additional Requirements:
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Method and Frequency of Class:
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Two to three lectures/seminars per week. Breakdown of hours: formal teaching - 25 hours approximately; outside reading, review and revision - 50 hours approximately.
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Method of Assessment:
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Two to three lectures/seminars per week. Breakdown of hours: formal teaching - 25 hours approximately; outside reading, review and revision - 50 hours approximately.
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Assessment Period:
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Assessed by end of Spring Semester
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