Congratulations to the winners of the SMBE 2018 annual faculty awards!
2018 SMBE Allan Wilson Junior Award for Independent Research Winner: Melissa Wilson Sayres, Arizona State University
Dr. Melissa Wilson Sayres is an Assistant Professor in the School of Life Sciences and Center for Evolution and Medicine at Arizona State University. Broadly, her laboratory analyzes large-scale genomic and transcriptomic datasets to study sex-specific processes. The Wilson Sayres laboratory studies how sex chromosomes arise and evolve, utilizes sex chromosomes to understand population history, and is working to incorporate genetic and phenotypic sex as a biological variable in health and disease research. She received her B.S. in Medical Mathematics from Creighton University in Omaha, Nebraska, her Ph.D. in Integrative Biology: Bioinformatics & Genomics from The Pennsylvania State University working with Dr. Kateryna Makova, and studied as a Miller postdoctoral fellow at the University of California, Berkeley with Rasmus Nielsen. Her laboratory and research are currently supported by an NIH NIGMS R35 Maximizing Investigators’ Research Award, the Leakey Foundation, and a Heritage grant from Arizona Game and Fish.
2018 Margaret Dayhoff Mid-Career Award Winner: Matthew W. Hahn
Matthew W. Hahn is a Professor of Biology and Computer Science at Indiana University. He got his B.S. from Cornell University working with Rick Harrison, his Ph.D. from Duke University working with Mark Rausher, and was a postdoctoral fellow at the University of California, Davis working with Chuck Langley and John Gillespie. His research uses population genetic and phylogenetic approaches to understand adaptation, speciation, and the evolution of genes and genomes.
2018 SMBE Motoo Kimura Lifetime Contribution Award Winner: Tomoko Ohta
I was born in 1933, and graduated from the University of Tokyo in 1956. At that time, female students were very few in Japanese Universities, and it was difficult to get a good job in a professional field. I spent a few years at the publishing company doing editorial tasks such as proof-reading. I was not good at this job and was looking for a research position at a university or an institute. Fortunately, the Kihara Institute for Biological Research moved from Kyoto to Yokohama and I was hired. There I worked on plant cytogenetics. Then I had a chance to study at North Carolina State University. After finishing my PhD in 1966, I found a position at the Kimura Laboratory of the National Institute of Genetics, Mishima, Japan, where I started research life on molecular evolution and population genetics. It was a good time to start research in this field, because Kimura was thinking to examine biochemical data from the standpoint of population genetics. He proposed the neutral theory of molecular evolution in 1968. In examining the neutral theory of molecular evolution, I was puzzled by three problems. 1: What are borderline mutations between the selected and the neutral mutations? 2: Why the molecular evolutionary rate depends on year rather than generation time? 3: Why heterozygosity is relatively insensitive to population size? I found that, by incorporating nearly neutral mutations, mostly slightly deleterious, between the selected and the neutral classes, one may explain the questions. I published the theory in 1973. In this century, genome data have tremendously increased and they tend to support the neutral and nearly neutral theories. Genome projects and genome diversity projects have been influential. The range of near-neutrality depends on protein structure and function. Now molecular systems on dynamic protein folding and degradation are being clarified, which suggest versatile nature of protein function.
Recent progress on gene regulation at the molecular level is remarkable. It is now clear that gene regulation depends upon numerous molecular machineries involved in chromatin structure and function. Until recently it has been thought that transcription factor binding to the specific regulatory region mainly controls gene expression. Now it is known that chromatin accessibility is important for transcription factor binding. Chromatin is mainly composed of histones and DNA, and very important for epigenetic processes. The epigenetic phenomena are very complicated and linked to various modification of chromatin components, i.e., DNA methylation, histone methylation, phosphorylation, acetylation, etc. Together with such modifications, RNA and non-histone proteins participate in controlling chromatin structure and function.
Let us consider how the new knowledge on gene expression relates to the neutral and nearly neutral theories. Sometime ago, gene regulatory systems were recognized to be robust. To be robust implies that the system is insensitive to mutations and other perturbations, and is thought to be caused by complex connections of gene expression pathways. I considered that this idea is important to make the range of near-neutrality larger, and hence the contribution of nearly neutral mutations becomes larger. It is now evident that numerous molecular machineries on chromatin structure and function are responsible for robustness. Many of the amino acid substitutions of a component protein of molecular machineries of chromatin are thought to have very small effects and become nearly neutral. Of course some amino acid substitutions may have a significant effect on gene expression or other chromatin functions, and natural selection determines their fate. It is amazing to see that genetic systems are remarkably complex but at the same time versatile. It is difficult to imagine how such complex systems could have evolved. Noteworthy is the fact that various subsystems are repeatedly utilized in evolution. It is important to recognize that these subsystems often have self-organizing properties. Then it is not needed to build subsystems from individual components. I am lucky that I have lived long enough to see such progress in our field, and continue my study at the Akashi Laboratory of the National Institute of Genetics, Japan.