Daryl D. Hurd

Dr. Hurd's research interests lie in understanding how genes and cells develop into an organism that senses and interacts with its environment. He uses the model C. elegans (a nematode roundworm) to study a particular set of genes that function in the nervous system. By deleting these genes and/or adding tagged versions of these genes, he seeks to understand how specific genes and cells contribute to sensory function, motor function and behavior.

Teaching

• BIOL 308 - Cell Biology
• BIOL 403 - Developmental Biology

Research

The recent sequencing of the genomes of the major biological model systems including humans has ushered in the genomic era in biology. Driven by technological advances in computing and imaging, biologists now approach problems in a holistic way. 'Omics' is the study of the entire body (the ome) of biological entities, and understanding how the genome, which is the entire body of genetic material, influences the phenome, which is the entire range of characteristics, has become biology's goal. Despite technological advance, full understanding of a complex biological process like the genetic control of animal development and behavior remains an elusive goal.

Model animal organisms such as Caenorhabditis elegans (a free-living nematode roundworm) continue to lead research efforts to understand development and behavior due primarily to ease of genetic manipulation and a host of other attractive features including a simple body plan, a short generation time and inexpensive culture. Within each of these model organisms, certain tissues or organs are particularly well-studied and knowledge of their development and function has provided insight into the genetic control of these processes and disease states in more complex organisms such as humans. In C. elegans for example, the development and function of the nervous system has attracted the attention of researchers for more than four decades.

How do genes/cells accomplish a program of specialized development and function that leads to normal behavior? I study two classes of genes, tubulins and kinases, in an effort to understand their contribution to sensory and motor function. Tubulins are part of a cell’s internal skeleton, while kinases are regulators of a broad variety of processes. Removal of some these genes singly or in combination causes defects in sensory and motor function, while tagged versions reveal that they are produced by nervous tissue. Some of my work is done in collaboration with Dr. Douglas Portman in the Center for Neural Development and Disease at the University of Rochester Medical Center.

Publications

• Hurd, D. D., R. M. Miller, L. Núñez and D. S. Portman. Specific alpha- and beta-tubulin isotypes optimize the functions of sensory cilia in C.elegans. Genetics 185: 883-896 (2010).
• Hurd, D. D. A microcosm of the biomedical research experience for upper level undergraduates. CBE-Life Sciences Education 7: 210-219 (2008).
• Hurd, D. D. and K. J. Kemphues. PAR-1 is required for morphogenesis of the Caenorhabditis elegans vulva. Developmental Biology 253: 54-65 (2003).
• O’Connell, K. F., C. Caron, D. D. Hurd, K. J. Kemphues, Y. Li and J. G. White. The C. elegans zyg-1 gene encodes a novel regulator of centrosome duplication with distinct maternal and paternal roles in the embryo. Cell 105: 547-558 (2001).
• Yager, J. S. Richards, D. S. Hekmat-Scafe, D. D. Hurd, V. Sundaresan, D. R. Caprette, W. M. Saxton, J. R. Carlson and M. Stern. Control of Drosophila perineurial glial growth by interacting neurotransmitter-mediated signaling pathways Proceedings of the National Academy of Sciences 98: 10445-10450 (2001).
• Martin, M. A. E., D. D. Hurd and W. M. Saxton. Kinesins in the nervous system. Cellular and Molecular Life Sciences 56: 200-216 (1999).
• Hurd, D. D. and W. M. Saxton. Kinesin mutations cause motor neuron disease phenotypes by disrupting fast axonal transport in Drosophila. Genetics 144: 1075-1085 (1996).
• Hurd, D. D., M. Stern and W. M. Saxton. Mutation of the axonal transport motor kinesin suppresses Shaker and enhances paralytic mutations in Drosophila. Genetics 142: 195-204 (1996).