Lecture

DNA Mutations: Mechanisms and Consequences

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In course

BIOENG-110: General Biology

Le but du cours est de fournir un aperçu général de la biologie des cellules et des organismes. Nous en discuterons dans le contexte de la vie des cellules et des organismes, en mettant l'accent sur les principes de réglementation que vous rencontrerez dan ...

Description

This lecture covers the mechanisms behind DNA mutations, including spontaneous mutations due to replication errors and tautomeric shifts in nucleotides. It also explores induced mutations caused by mutagens like chemicals, radiation, and reactive oxygen species. The consequences of these mutations, such as base pair mismatches and DNA breaks, are discussed, along with repair mechanisms. The lecture emphasizes the inevitability of mutations and their role in genetic diversity.

Instructors (5)

Camille Véronique Bernadette Goemans

Camille's research focuses on understanding how antibiotics and non-antibiotic drugs affect the diverse bacteria from the human gut microbiota and how they contribute to dysbiosis and the development of antibiotic resistance. To achieve this goal, she combines systems approaches with molecular microbiology, bacterial genetics and biochemistry.She obtained her Bachelor's and Master's degrees in Biomedical Sciences from the UCLouvain, Belgium, after which she completed her PhD (FRIA national fellowship) at th

Freddy Radtke

Freddy Radtke obtained his Ph.D. in Molecular Biology from the University of Zürich in 1994. In 1995, he started his postdoctoral research in the laboratory of Michel Aguet at Genentech, Inc. (San Francisco, USA). In 1997, he returned to Switzerland with Michel Aguet and finished his postdoctoral fellowship at the Swiss Institute for Experimental Cancer Research (ISREC) in Lausanne. From 1999‑2005, he was a group leader and Associate Member at the Ludwig Institute for Cancer Research. Freddy Radtke then joined ISREC in January 2006 as a senior scientist and in July 2006, he was appointed Associate Professor at the EPFL School of Life Sciences

Viesturs Simanis

Viesturs Simanis was awarded a degree in Biochemistry from Imperial College London. He carried out his doctoral studies with David Lane at Imperial College, London University, and postdoctoral studies with Paul Nurse (London and Oxford). He has been a group leader at ISREC since 1988. In 2006 he was appointed Associate Professor at the EPFL School of Life Sciences

Kristina Schoonjans

Expertise Bile acid signalingNutrient sensingIntermediary metabolismMetabolic disorders Teaching & PhD PhD Students Adrien Faure Past EPFL PhD Students Pan Xu, Ece Yildiz, Nadia Bresciani, Yu Sun, Francesca Pontanari, Alejandro Alonso Calleja Past EPFL PhD Students as codirector Mitsunori Nomura, Pan Xu, Katyayanee Neopane, Lucie Camille Chanvillard, Jakob Josef Langer, Bilge Sen Elçi Courses General Biology BIOENG-110 The purpose of the course is to provide a general overview of the biolo

Johannes Gräff

Official source

Related concepts (29)

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.

Frameshift mutation

A frameshift mutation (also called a framing error or a reading frame shift) is a genetic mutation caused by indels (insertions or deletions) of a number of nucleotides in a DNA sequence that is not divisible by three. Due to the triplet nature of gene expression by codons, the insertion or deletion can change the reading frame (the grouping of the codons), resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein.

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.

Germline mutation

A germline mutation, or germinal mutation, is any detectable variation within germ cells (cells that, when fully developed, become sperm and ova). Mutations in these cells are the only mutations that can be passed on to offspring, when either a mutated sperm or oocyte come together to form a zygote. After this fertilization event occurs, germ cells divide rapidly to produce all of the cells in the body, causing this mutation to be present in every somatic and germline cell in the offspring; this is also known as a constitutional mutation.

Nonsense mutation

In genetics, a nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and in leading to a truncated, incomplete, and nonfunctional protein product. Nonsense mutation is not always harmful, the functional effect of a nonsense mutation depends on many aspects, such as the location of the stop codon within the coding DNA. For example, the effect of a nonsense mutation depends on the proximity of the nonsense mutation to the original stop codon, and the degree to which functional subdomains of the protein are affected.

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