Abstract:
:Although the anti-apoptotic activity of Bcl-2 has been extensively studied, its mode of action is still incompletely understood. In the nematode Caenorhabditis elegans, 131 of 1090 somatic cells undergo programmed cell death during development. Transgenic expression of human Bcl-2 reduced cell death during nematode development, and partially complemented mutation of ced-9, indicating that Bcl-2 can functionally interact with the nematode cell death machinery. Identification of the nematode target(s) of Bcl-2 inhibition would help clarify the mechanism by which Bcl-2 suppresses apoptosis in mammalian cells. Exploiting yeast-based systems and biochemical assays, we analysed the ability of Bcl-2 to interact with and regulate the activity of nematode apoptosis proteins. Unlike CED-9, Bcl-2 could not directly associate with the caspase-activating adaptor protein CED-4, nor could it inhibit CED-4-dependent yeast death. By contrast, Bcl-2 could bind the C. elegans pro-apoptotic BH3-only Bcl-2 family member EGL-1. These data prompt us to hypothesise that Bcl-2 might suppress nematode cell death by preventing EGL-1 from antagonising CED-9, rather than by inhibiting CED-4.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Jabbour AM,Puryer MA,Yu JY,Lithgow T,Riffkin CD,Ashley DM,Vaux DL,Ekert PG,Hawkins CJdoi
10.1242/jcs.02985subject
Has Abstractpub_date
2006-06-15 00:00:00pages
2572-82issue
Pt 12eissn
0021-9533issn
1477-9137pii
jcs.02985journal_volume
119pub_type
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