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Lecture

Molecular Evolution: Repair Mechanisms and Genetic Diversity

In course

ENV-103: Biology

This course will cover the fundamental principles governing life and the living world. Topics will include the diversity of living organisms, cellular biology, genetics, evolution, and ecology. This course provides a foundation in biology, fostering critic ...

Description

This lecture covers the molecular mechanisms of defense, mutations, and variants, including DNA repair mechanisms such as proofreading and mismatch repair. It also delves into the CRISPR/Cas system, homologous recombination, and the evolution of DNA repair systems. The historical context of restriction/modification systems and the groundbreaking work of researchers like Werner Arber, Daniel Nathans, and Hamilton Smith are discussed. The lecture further explores the long-term experimental evolution of E. coli by Richard Lenski, highlighting the emergence of new traits and species over thousands of generations.

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Instructors (4)

Anna Carratala Ripolles

During my PhD, I mainly focused on characterizing the effect of environmental factors (namely temperature and sunlight) and disinfectants on the stability of human viral pathogens as contaminants of aquatic environments. In addition,I developed a novel source tracking tool to identify avian fecal contamination in environmental samples. Thanks to a research fellowship given by the Spanish Ministry of Science and Technology, I also had the opportunity to explore the diversity of marine viruses in Mediterranean coastal waters by genetic fingerprinting and by next generation sequencing. Later on, I became interested in the long-term effect of environmental stressors on virus communities, so I joined the LCE as a postdoc to investigate the adaptation of enteroviruses to ultraviolet radiation. For 4 years, I worked on developing UV-resistant viruses and characterizing their acquired phenotypic and genetic properties by combining directed evolution experiments, deep sequencing and population genetics. Out of the lab, I am passionate about nature, traveling and scuba diving.

Julien Maillard

2011 - present: Research associate at the Laboratory for Environmental Biotechnology (LBE, IIE-ENAC, EPFL) 2007 - 2010: Postdoctoral Fellow at the Laboratory for Environmental Biotechnology (LBE, IIE-ENAC, EPFL) 2005 - 2006: Postdoctoral Fellow at the University of East Anglia (UEA, Norwich, UK) 2000 - 2004: PhD thesis at the Laboratory for Environmental Biotechnology (LBE) 1995 - 2000: B.sc & M.sc at the Swiss Federal Institute for Technology, Zurich (ETHZ)

Ianina Altshuler

Pierre Rossi

Official source

Ontological neighbourhood

Biology

Genetics: Population genetics

Related concepts (32)

DNA repair

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in tens of thousands of individual molecular lesions per cell per day. Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell's ability to transcribe the gene that the affected DNA encodes.

Mutation

In biology, a mutation is an alteration in the nucleic acid sequence of the genome of an organism, virus, or extrachromosomal DNA. Viral genomes contain either DNA or RNA. Mutations result from errors during DNA or viral replication, mitosis, or meiosis or other types of damage to DNA (such as pyrimidine dimers caused by exposure to ultraviolet radiation), which then may undergo error-prone repair (especially microhomology-mediated end joining), cause an error during other forms of repair, or cause an error during replication (translesion synthesis).

Base excision repair

Base excision repair (BER) is a cellular mechanism, studied in the fields of biochemistry and genetics, that repairs damaged DNA throughout the cell cycle. It is responsible primarily for removing small, non-helix-distorting base lesions from the genome. The related nucleotide excision repair pathway repairs bulky helix-distorting lesions. BER is important for removing damaged bases that could otherwise cause mutations by mispairing or lead to breaks in DNA during replication.

Nucleotide excision repair

Nucleotide excision repair is a DNA repair mechanism. DNA damage occurs constantly because of chemicals (e.g. intercalating agents), radiation and other mutagens. Three excision repair pathways exist to repair single stranded DNA damage: Nucleotide excision repair (NER), base excision repair (BER), and DNA mismatch repair (MMR). While the BER pathway can recognize specific non-bulky lesions in DNA, it can correct only damaged bases that are removed by specific glycosylases.

Point mutation

A point mutation is a genetic mutation where a single nucleotide base is changed, inserted or deleted from a DNA or RNA sequence of an organism's genome. Point mutations have a variety of effects on the downstream protein product—consequences that are moderately predictable based upon the specifics of the mutation. These consequences can range from no effect (e.g. synonymous mutations) to deleterious effects (e.g. frameshift mutations), with regard to protein production, composition, and function.

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