Professor of Biology
B.A., Kansas State University
Ph.D., University of California, San Francisco
Member of: Institute of Molecular Biology
Office: Streisinger Hall Room 375E
Lab: Streisinger Hall Room 375
- Meiotic and Mitotic Spindle Assembly and Function, and Cytokinesis, in the early Caenorhabditis elegans embryo
- Cell Polarity in the early Caenorhabditis elegans embryo
The Bowerman lab uses genetics, molecular biology, and microscopy to study cytoskeletal regulation and function in the early Caenorhabditis elegans embryo. Beginning with the first mitotic cell division, the early embryo undergoes a sequence of five asymmetric cleavages. Figure 1 shows the first three mitotic divisions during embryogenesis; two of these are asymmetric.
These early divisions are largely responsible for establishing the pattern of cell fates required for normal embryonic development. The asymmetric divisions, with their stereotyped timing and mitotic spindle positioning, provide a rich context in which to use the powerful genetics of C. elegans to investigate cytoskeletal function.
The actomyosin cytoskeleton, including the non-muscle myosin II called NMY-2 (in red in the late anaphase mitotic one-cell stage embryo in Figure 2), is localized predominantly at the cell cortex. The actomyosin cytoskeleton is important both for generating anterior-posterior polarity, and for the execution of cytokinesis.
Microtubules (shown in green in Figure 2; DNA is in blue) form the meiotic and mitotic spindles, which capture and segregate chromosomes. During mitosis, astral microtubules contact the cell cortex and are important for proper spindle positioning. Current C. elegans research projects in the lab focus on the assembly and function of meiotic and mitotic spindles, cell polarity, cytokinesis, and mitotic spindle orientation in early embryonic cells.
Go to our lab website to see more information on our research and movies of wild-type and mutant early embryonic cell divisions.
S. M. O’Rourke, J. Yochem, A. Connolly, M. H. Price, L. Carter, J. Lowry, D. W. Turnbull, N. Kamps-Hughes, N. Stiffler, M. R. Miller, E. A. Johnson and B. Bowerman (2011). Two rapid methods for mapping and identifying mutation in C. elegans: RAD mapping and genomic interval pull-down sequencing. Genetics 189, 767-778.
S. M. O’Rourke, C. Carter, L. Carter, S. N. Christensen, M. Jones, B. Nash, M. Price, D. Turnbull, A. Garner, D. R. Hamill, V. R. Osterberg, R. Lyczak, E. E. Madison, M. Nguyen, N. Sandberg, N. Sedghi, J. H. Willis, J. Yochem, E. A. Johnson and B. Bowerman (2011). A survey of new temperature-sensitive, embryonic-lethal mutations in C. elegans: 25 alleles of thirteen genes. Public Library of Science One 6(3), e16644.
L. Chen, Z. Wang, A. Ghosh-Roy, T. Humbert, D. Yan, S. O. O’Rourke, B. Bowerman, Z. Wu, Y. Jin and A. D. Chisholm (2011). Novel axon regeneration pathways identified by systematic genetic screening in C. elegans. Neuron 71, 1043-1057.
S. M. O’Rourke, S. N. Christensen and B. Bowerman (2010). C. elegans EFA-6 limits microtubule growth at the cell cortex. Nature Cell Biology 12, 1235-1240
M. Dorfman, J.-E. Gomes, S. O. O’Rourke and B. Bowerman (2009). Using RNA interference to identify specific modifiers of a temperature-sensitive, embryonic-lethal mutation in the C. elegans ubiquitin-like Nedd8 protein modification pathway gene rfl-1. Genetics 182, 1035-1049.
W. Q. Gillis, B. A. Bowerman and S. Q. Schneider (2009). Whole genome duplications and expansion of the vertebrate GATA transcription factor gene family. BMC Evolutionary Biology 9, 207.