February 22, 2024
Stephen Miller to present Division of Biology Seminar
Submitted by Division of Biology
Stephen Miller, associate professor of biological sciences, University of Maryland – Baltimore County will present "Simple Steps to Complexity? Investigating Developmental Mechanisms and Their Origins in the Volvocine Green Algae" as part of the Division of Biology Seminar Series at 3:30 p.m. Monday, Feb. 26, in Room 221 of Ackert Hall.
Multicellularity has arisen independently in many eukaryotic lineages, but little is known about the mechanisms that drive the transition from unicellular to differentiated multicellular life. The volvocine green algae, which include unicellular and undifferentiated, partially differentiated, and fully differentiated species comprise an excellent system for investigating the genetic pathways involved in the evolution of developmental complexity. The best studied multicellular member of this family, Volvox carteri, possesses just two distinct cell types: small, terminally differentiated somatic cells and large reproductive cells called gonidia. Progenitors of these two cell types are set aside by symmetric and asymmetric embryonic cell divisions that collectively generate approximately 16 presumptive gonidia and about 2000 presumptive somatic cells.
Miller's lab investigates the mechanisms that control the production of these cell types, and how those mechanisms evolved. One line of investigation involves a J-protein chaperone (GlsA) and its retinoblastoma-protein pathway binding partner (Dp1) in regulation of cell division symmetry and cell number. Previously we showed that GlsA is essential for asymmetric cell division, and recently we found that CRISPR-generated dp1 mutants make aberrant asymmetric cell divisions, and fewer cell divisions than the wild type, indicating that Dp1 is essential for normal division symmetry and number.
A second line of investigation in Miller's lab involves analysis of RegA, a putative transcription factor that is essential for maintenance of the somatic cell fate, and of close RegA paralogs. Results from domain swap, overexpression, and RNA-seq experiments suggest that somatic cell differentiation evolved in V. carteri when an ancestral gene that repressed cell growth in response to nutrient limitation duplicated, and the duplicate now known as RegA evolved to repress growth in a developmental context to prevent cells from enlarging enough to reproduce. These and other findings suggest the idea that at least in some cases new developmental traits evolved in the volvocine lineage through relatively minor changes to an ancestral genetic toolkit.
If you would like to visit with Miller, please contact Brad Olson at bjsco@k-state.edu.