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A suppressor screen is used to identify suppressor mutations that alleviate or revert the phenotype of the original mutation, in a process defined as synthetic viability. [13] Suppressor mutations can be described as second mutations at a site on the chromosome distinct from the mutation under study, which suppress the phenotype of the original ...
Early studies in Caenorhabditis elegans [1] and Drosophila melanogaster [2] [3] saw large-scale, systematic loss of function (LOF) screens performed through saturation mutagenesis, demonstrating the potential of this approach to characterise genetic pathways and identify genes with unique and essential functions.
Types of mutations that can be introduced by random, site-directed, combinatorial, or insertional mutagenesis. In molecular biology, mutagenesis is an important laboratory technique whereby DNA mutations are deliberately engineered to produce libraries of mutant genes, proteins, strains of bacteria, or other genetically modified organisms.
More recently, large-scale phenotypic screens have also been used in animals, e.g. to study lesser understood phenotypes such as behavior. In one screen, the role of mutations in mice were studied in areas such as learning and memory, circadian rhythmicity, vision, responses to stress and response to psychostimulants.
Large-scale quantitative mutagenesis screens, in which thousands of millions of mutations are tested, invariably find that a larger fraction of mutations has harmful effects but always returns a number of beneficial mutations as well.
To provide examples of how Xenbase could be used to facilitate academic research, two research articles are briefly described below. Genetic Screens for Mutations Affecting Development of X. tropicalis. [14] This paper uses Xenbase resources to create and characterize mutations in Xenopus tropicalis. Goda et al., performed a large scale forward ...
Classical geneticists would have used phenotypic traits to map the new mutant alleles. Eventually the hope is that such screens would reach a large enough scale that most or all newly generated mutations would represent a second hit of a locus, essentially saturating the genome with mutations.
A large-scale screen for somatic mutations in breast and colorectal tumors showed that many low-frequency mutations each make small contribution to cell survival. [33] If cell survival is determined by many mutations of small effect, it is unlikely that genome sequencing will uncover a single "Achilles heel" target for anti-cancer drugs.