Abstract
Understanding the biology of C. elegans relies on identification and analysis of essential genes, genes required for growth to a fertile adult. Approaches for identifying essential genes include several types of classical forward genetic screens, genome-wide RNA interference screens and systematic targeted gene knockout. Based on most estimates made from screening results thus far, from 15-30% of C. elegans genes appear to be essential. Genetic redundancy masks some essential functions and pleiotropy of many essential genes poses a challenge for a full understanding of their functions. Temperature sensitive mutations are valuable tools for studies of essential genes, but our ability to analyze essential genes would benefit from development of new tools for conditional inactivation or activation of specific genes.
Highlights
There are three types of mutations that identify essential functions: zygotic lethal mutations, maternal-effect lethal mutations and sterile mutations
Most lethal and sterile mutations have been identified by random mutagenesis followed by either of two types of screens: genome-wide screens for conditional lethals, such as temperature-sensitive mutations, and screens for non-conditional lethals and steriles in particular genomic regions for which balancers are available
The number of essential genes in C. elegans as estimated by gene knockout, RNA interference (RNAi) and classical genetic screens appears to be less than 30% of the genome
Summary
There are three types of mutations that identify essential functions: zygotic lethal mutations (lethals), maternal-effect lethal mutations (maternal-effect lethals) and sterile mutations (steriles). Zygotic lethals prevent the development to adult of individuals homozygous for the mutation. Zygotic lethals are broadly categorized, based on the time of developmental arrest, as embryonic or larval lethals. Maternal-effect lethals are a special class of sterilizing mutations that prevent the development of the progeny of hermaphrodites homozygous for the mutation. Such mutations define genes whose expression in the mother is required for embryonic development. Sterile mutations prevent the production of fertilized eggs by individuals homozygous for the mutation. Sterility could arise due to defects in germline development, somatic gonad development, oogenesis, spermatogenesis, ovulation or fertilization
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