Ageing, Sex and DNA Repair (20)
Code | School | Level | Credits | Semesters |
LIFE3128 | Life Sciences | 3 | 20 | Autumn UK |
- Code
- LIFE3128
- School
- Life Sciences
- Level
- 3
- Credits
- 20
- Semesters
- Autumn UK
Summary
Why do we age and succumb to cancer? Has human civilization exposed a process of cellular decay for which evolution never prepared us? To cope with the continuous exposure to mutagens and carcinogens of both natural and human origin, our cells have evolved mechanisms to maintain the genome intact from one generation to the next. However, the age-related onset of cancer provides a stark reminder that we cannot avoid damage to the genetic blueprint on which life depends. The inherited disorders that lead to premature ageing, and the extent to which genetic variation impacts upon natural cell senescence, suggest 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. The process of sexual reproduction is underpinned by homologous recombination, which shuffles the genome and ensures correct chromosome segregation in meiosis, thereby contributing to genetic diversity. 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, and in human populations, have uncovered the relationships between genetic diversity, somatic ageing, DNA repair, and the necessity to maintain an intact genome from one generation to the next. 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 in humans.
Target Students
Honours Biology, Biochemistry, Genetics, Zoology, Natural Sciences, Microbiology and Biotechnology.Available to JYA/Erasmus students.
Classes
This module may be delivered through lectures, seminars, workshops and labs etc
Assessment
- 40% Assessment 1: Summative 'journal club' presentation.
- 60% Exam 1 (2-hour): Essay exam.
Assessed by end of designated period
Learning Outcomes
To understand current theories of ageing and DNA repair, how these processes may be related, and to understand the causes of genetic damage that may arise from endogenous and exogenous sources
To understand the variety and extent of diversity in human DNA, and the techniques used for observing mutations in humans.
To understand the diverse cellular mechanisms that have evolved to repair DNA damage in bacteria and eukaryotes, and how these mechanisms are coordinated with the cell cycle.
To understand how defects in DNA repair processes, and in the cell cycle, may lead to mutation, and to cancer, ageing and death in humans.
To understand how homologous recombination is used to ensure accurate chromosome segregation in meiosis, and how it contributes to genetic diversity in humans.
To understand how error-prone DNA repair processes are used to ensure genetic diversity in the mammalian immune system.