The regulation of programmed and pathological cell death in C. elegans

Programmed cell death, or apoptosis, is important in the development and homeostasis of metazoans. In the nematode C. elegans, four genes, egl-1, ced-9, ced-4, and ced-3, constitute the core pathway acting in all somatic programmed cell deaths. This pathway is evolutionarily conserved in humans. The BH3-only protein EGL-1 is transcriptionally upregulated in cells fated to undergo programmed cell death, and EGL-1 blocks cell-death inhibition by the cell-death regulator CED-9, a Bcl-2 family member. The binding of EGL- 1 to CED-9 releases the Apaf- 1-like adaptor protein CED-4 from CED-9, so that CED-4 can activate the caspase CED-3, a protease that is the effector of programmed cell death. In this thesis, I describe three projects, each of which examines one aspect of C. elegans cell death. From. screens for mutations that increase cell death in a sensitized genetic background, I identified a gene that protects cells from programmed cell death.

Department dc:contributor.department

Massachusetts Institute of Technology. Dept. of Biology.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2007

Author dc:creator

• Galvin, Brendan D. (Brendan Daniel)

Advisor dc:contributor.advisor

• H. Robert Horvitz.

• Biology.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/38633

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/38633