|Department:||Department of Plant, Soil and Entomological Sciences|
|Credentials:||1980 - Ph.D., University of Iowa, Department of Zoology (Genetics)|
University of Idaho
875 Perimeter Dr.
PO Box 442339
Moscow, ID 83844-2339
Autophagy and its paradoxical contributions to both pro-life and pro-death processes in cells.
Autophagic cell death: With a few exceptions, eukaryotic cells of every kind and kingdom maintain superficially redundant cell death programs. One, called apoptosis, allows cells to die without leaking metabolic products that might poison cells adjacent to them. The other, which, for many years, was seen as the only alternative to apoptosis, was necrosis, an uncontrolled form of death that leads to the breakdown of cellular membranes and release of everything inside. Recently, some researchers acknowledged a third cell death pathway called autophagic cell death (ACD), but this contention has remained controversial. Autophagy normally operates during starvation or biotic stress to harvest cytoplasm, or ribosomes, or peroxisomes as needed, so that they can be broken down in to the raw amino acids and lipids that make them up. During ACD, cells purportedly re-direct autophagy to kill cells either by over-harvesting cell material, or alternatively, selectively harvesting proteins that keep apoptosis and necrosis in check. At this time, we do know which of these alternatives, if either, applies. My group believes we have found a way to fill in some of the blanks by studying ACD in a convenient model organism, that common beer and bread yeast, Saccharomyces cerevisiae. Our goal is to use this system to identify how cells select which death process to use in different adverse situations, and to identify the genes responsible for ACD. History has shown that what is true for yeast, is very often true for other eukaryotes including animals and plants. For this reason, we believe that these studies have the potential to help us understand processes that affect us all including the struggle to remain biologically youthful and resistant to a host of deadly pathogens that trigger cell death as part of their normal lifecycle.
Kolodziejek, A. M., et al. (2013). "Physiological levels of glucose induce membrane vesicle secretion and affect the lipid and protein composition of Yersinia pestis cell surfaces." Appl Environ Microbiol 79(14): 4509-4514.
Dziedzic, S.A. and Caplan, A., 2012. Autophagy proteins play cytoprotective and cytocidal roles in leucine starvation-induced cell death in Saccharomyces cerevisiae. Autophagy 8:731-738.
Dziedzic, S.A. and Caplan, A., 2011. Identification of autophagy genes participating in zinc-induced necrotic cell death in Saccharomyces cerevisiae. Autophagy 7:490-500.
Iyer, S. and Caplan, A. 1998. Products of proline catabolism can function as pleiotropic effectors in rice. Plant Physiol. 116:203-211.
Crespi, M., Messens, E., Caplan, A., Van Montagu, M., and Desomer, J. 1992. Fasciation induction by the phytopathogen Rhodococcus fasciens depends upon a linear plasmid encoding a cytokinin synthase gene. EMBO J. 11:795-804.
Masuta, C., Van den Bulcke, M., Bauw, G., Van Montagu, M., and Caplan, A., 1991. Differential effects of elicitors on the hypersensitive response of rice. Plant Physiol. 97:619-629.
Center for Reproductive Biology cited as author affiliation