Dr. Sarah Zanders
Department of Molecular & Integrative Physiology
Stowers Institute for Medical Research
United States of America
Biography
Sarah Zanders, Ph.D., assistant investigator, is fascinated by selfish genes. Unlike the genes that encode for proteins crucial to healthy function of an organism, such as insulin and collagen, selfish genes “have no apparent redeeming features,” Zanders says. They’re considered parasites, Zanders says, because they do not promote the overall fitness of the organism. Their sole function appears to be to promote their own survival by ensuring their presence in the genomes of the offspring of an organism. Selfish genes, which are the products of random mutations generating new genes, or novel variants of existing genes, can short-circuit natural selection. “By cheating the process of sexual reproduction, selfish genes persist and spread in populations,” says Zanders. Zanders provides a simple explanation of how selfish genes may behave during meiosis, the specialized form of cell division that creates gametes, like eggs and sperm. During meiosis, a male normally produces an equal number of sperm bearing an X chromosome as sperm carrying a Y chromosome.
Research Interest
Our laboratory uses an evolution-guided molecular approach to understand the causes of infertility. In particular, we are interested in the effects of genetic conflicts caused by selfish components embedded in eukaryotic genomes. These parasitic components include transposable elements, which can proliferate by copying and pasting themselves into new regions of the genome, as well as meiotic drive alleles. Meiotic drive alleles persist and spread in populations by biasing their transmission into functional gametes (reproductive cell such as sperm). For example, a meiotic drive allele on a male’s (XY) X chromosome could drive the male to father exclusively daughters by generating only X-bearing sperm. Transposons and meiotic drive alleles can cause infertility, but the molecular mechanisms by which they act in meiosis are not well understood. Our research proposes that conflicts driven by these parasites are major drivers of genome evolution.
