Adi Stern
Adi is a post-doc working with Raul Andino in UCSF and Rasmus Berkeley in UC Berkeley. Her interests lie in understanding the “arms-race” evolution of viruses and their hosts. Adi received a B.Sc. in Biology and Psychology, and an additional B.Sc. in Math, from Tel-Aviv University. In her PhD research with Tal Pupko, she developed phylogenetic models of evolution, and used them to study adaptationin different HIV strains. Next, during a postdoc in the Weizmann institute with Rotem Sorek, she studied the evolution of the CRISPR antiviral system, and documented diversity of phages and CRISPRs in the human gut microbiome. Currently, Adi combines population genetics theory with experimental evolution to study the constraints governing the evolution of “mutant-clouds” of RNA viruses. In Oct. 2014 Adi is starting a research group in Tel Aviv University, where she plans to continue combining theory with experimental evolution to study how viruses of all types and forms adapt to continuously changing environments. For more information, have a look at her website.
Talk: Costs and benefits of mutational robustness
Hidden genetic variability, in the form of neutral mutations, is thought to facilitate evolution by providing a reservoir of potentially adaptive alleles. Mutational robustness, which is the ability of a population to buffer deleterious mutations, determines the neutral variability in a population. Here we focus on a particular type of robustness, namely multiple viruses replicating in the same cell. During high multiplicity of infection (MOI), complementation between virus variants can buffer the effect of detrimental mutations. We examine this prediction by comparing populations of RNA viruses grown at high or low MOI. Comparison of the minor allele composition of these populations demonstrated that indeed high MOI buffers detrimental mutations. Next, guided by these experimental results, we developed a theoretical framework to compare the evolutionary behavior of robust viral populations and non-robust, i.e. brittle, populations as they adapt to the challenges of an environmental change. We find that robust populations adapt more rapidly but purge novel deleterious mutations more slowly. Brittle populations are better prepared to adapt if neutral alleles in a given environment become predominantly deleterious in a new environment. Whether mutational robustness facilitates or hinders adaptation to a new condition depends on the ratio of beneficial to detrimental mutations hidden within the “neutral” genetic variability in the starting population. We illustrate different types of environmental changes where mutational robustness, or lack there of, plays a role in viral adaptation. Thus, under certain conditions, diversity may actually be an impediment for viral adaptation.
Seminar details
Wednesday April 9th, 2014
1:00 PM Lunch (sign up below)
1:15 PM Seminar
Location: Clark Center S360
If you would like to speak with Adi, contact Pleuni Pennings (pleuni@stanford.edu)
CEHG Evolgenome 