Paul W. Sternberg is an American biologist. He does research for WormBase on C. elegans, a model organism.
Early life and education Paul Sternberg grew up in Long Island, New York. He attended Hampshire College for undergrad in Amherst, Massachusetts where he received his B.A. in 1978. After that he went to MIT where he received his PhD in Biology for work on nematode development with Robert Horvitz. He went on to do postdoctoral research with Ira Herskowitz in yeast molecular development at the University of California San Francisco. He is currently the Thomas Hunt Morgan Professor of Biology at the California Institute of Technology.
WormBase Sternberg is a Primary investigator for WormBase. WormBase is a data repository for nematode biology. C. elegans has been used in studies of development and neurobiology. WormBase has information from nine species and five are from the genus Caenorhabditis, one of which is C. elegans. WormBase provides: a genome browser, genome, gene and protein sets for searches on sequence similarities and gene and protein summaries.
Gene Ontology Consortium He also serves as a primary investigator for the Gene Ontology Consortium. The consortium provides knowledge on the functions of genes and gene products. It was founded in 1998 and is widely accepted in the life sciences. The Gene Ontology resource has the most comprehensive information about the functions of genes.”The ontology covers three distinct aspects of gene function: molecular function, cellular component, and biological process”.
Current research Sternberg is a coauthor on the article, "Autism-associated missense genetic variants impact locomotion and neurodevelopment in Caenorhabditis elegans" (2019). They used C. elegans as a genetic model to look for phenotypic missense alleles collected from autism spectrum disorder studies done in humans. Missense variants cause around half the genetic changes that are known to cause disease. They used CRISPR-Cas9 to generate C. elegans equivalent human missense mutants. They compared the phenotypes from the missense mutants to the wildtype and known loss-of-function mutant controls in the autism-associated missense alleles. They found that 70% of missense alleles showed evident phenotypic changes in locomotion, morphology, and fecundity. They used this method to show subtle phenotypic changes and the effect that missense mutations can have on human disease. They did find that 14 missense variants have a significant function in C. elegans orthologs of human genes.
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