June 23, 2010
UMMS researchers identify important receptor in autophagy during cell death
WORCESTER, Mass—Research published this week in Nature has enhanced the understanding of the dual roles of autophagy, a cellular developmental process that is associated with both hormone-regulated cell death and cell survival in response to starvation—roles that had previously been unclear to scientists. In a paper titled, “Activation of autophagy during cell death requires the engulfment receptor Draper,” published online June 24, researchers at the University of Massachusetts Medical School distinguish the two and describe a receptor responsible for autophagy during cell death. Autophagy, a process that targets cell components for degradation, is an important cellular response to starvation and stress, and plays essential roles in development, cell death, aging, immunity, neurodegeneration and cancer.
“Prior studies of yeast had identified conserved factors that regulate autophagy, but differences in the role of autophagy in specific cell types suggest that there may be specific regulators of autophagy in animals, including fruit flies, and humans,” said author Eric H. Baehrecke, PhD, professor of cancer biology at UMMS.
Autophagy degrades cytoplasmic components that are required for cell survival in response to starvation. Autophagy has also been associated with cell death, but it is unclear what may distinguish autophagy during cell survival and death. In the fruit fly Drosophila, salivary glands undergo programmed cell death that requires autophagy genes. This study shows that the evolutionarily conserved receptor Draper is required for autophagy during cell death. Surprisingly, Draper is required for autophagy induction in dying salivary gland cells, but does not regulate starvation-induced autophagy in cells where autophagy is known to promote cell survival. Draper is the first factor that distinguishes autophagy that is associated with cell death from cell survival.
“Scientists have been puzzled by how certain cells undergo autophagy during developmentally regulated cell death, while other cells use autophagy to survive during times of stress,” said Marion Zatz, Ph.D., who oversees programmed cell death grants at the NIH’s National Institute of General Medical Sciences, which funded the study. “This work for the first time distinguishes between autophagy’s dual roles by identifying a factor, Draper, that is required for autophagy in the context of developmentally programmed cell death but not in response to external cues for the survival response.”
Co-authors of the study are Christina K. McPhee, PhD, of the department of cancer biology at UMMS and the department of cell biology and molecular genetics at the University of Maryland; Mary A. Logan, PhD, of the department of neurobiology at UMMS; and Marc R. Freeman, PhD, associate professor of neurobiology at UMMS and Howard Hughes Medical Institute.
About the University of Massachusetts Medical School
The University of Massachusetts Medical School, one of the fastest growing academic health centers in the country, has built a reputation as a world-class research institution, consistently producing noteworthy advances in clinical and basic research. The Medical School attracts more than $240 million in research funding annually, 80 percent of which comes from federal funding sources. The mission of the Medical School is to advance the health and well-being of the people of the commonwealth and the world through pioneering education, research, public service and health care delivery with its clinical partner, UMass Memorial Health Care. For more information, visit www.umassmed.edu.
Contact: Public Affairs