TY - JOUR
T1 - Hid arbitrates collective cell death in the Drosophila wing
AU - Garcia-Hughes, Gianella
AU - Link, Nichole
AU - Ghosh, Anwesha B.
AU - Abrams, John M.
N1 - Funding Information:
This work was supported by NIH ( GM072124 and GM115682 ), the Welch Foundation ( I-1865 ), the Ellison Medical Foundation ( AG-SS-2743-11 ) and CPRIT ( RP110076 ). The authors thank Erin Regan for technical assistance, Abhijit Budge and Kate Luby-Phelps with the UT Southwestern Live Cell Imaging Facility for assistance with imaging, Bloomington Stock Center for fly strains, and Shamsideen Ojelade, Melissa O'Neal, Paula Kurtz, Annika Wylie, Alejandro D'Brot, and Po Chen for discussion.
Publisher Copyright:
© 2015 Elsevier B.V..
PY - 2015/11/1
Y1 - 2015/11/1
N2 - Elimination of cells and tissues by apoptosis is a highly conserved and tightly regulated process. In Drosophila, the entire wing epithelium is completely removed shortly after eclosion. The cells that make up this epithelium are collectively eliminated through a highly synchronized form of apoptotic cell death, involving canonical apoptosome genes. Here we present evidence that collective cell death does not require cell-cell contact and show that transcription of the IAP antagonist, head involution defective, is acutely induced in wing epithelial cells prior to this process. hid mRNAs accumulate to levels that exceed a component of the ribosome and likewise, Hid protein becomes highly abundant in these same cells. hid function is required for collective cell death, since loss of function mutants shows persisting wing epithelial cells and, furthermore, silencing of the hormone bursicon in the CNS produced collective cell death defective phenotypes manifested in the wing epithelium. Taken together, our observations suggest that acute induction of Hid primes wing epithelial cells for collective cell death and that Bursicon is a strong candidate to trigger this process, possibly by activating the abundant pool of Hid protein already present.
AB - Elimination of cells and tissues by apoptosis is a highly conserved and tightly regulated process. In Drosophila, the entire wing epithelium is completely removed shortly after eclosion. The cells that make up this epithelium are collectively eliminated through a highly synchronized form of apoptotic cell death, involving canonical apoptosome genes. Here we present evidence that collective cell death does not require cell-cell contact and show that transcription of the IAP antagonist, head involution defective, is acutely induced in wing epithelial cells prior to this process. hid mRNAs accumulate to levels that exceed a component of the ribosome and likewise, Hid protein becomes highly abundant in these same cells. hid function is required for collective cell death, since loss of function mutants shows persisting wing epithelial cells and, furthermore, silencing of the hormone bursicon in the CNS produced collective cell death defective phenotypes manifested in the wing epithelium. Taken together, our observations suggest that acute induction of Hid primes wing epithelial cells for collective cell death and that Bursicon is a strong candidate to trigger this process, possibly by activating the abundant pool of Hid protein already present.
KW - Apoptosis
KW - Collective cell death
KW - Development
KW - Eclosion
KW - Hormone
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U2 - 10.1016/j.mod.2015.07.008
DO - 10.1016/j.mod.2015.07.008
M3 - Article
C2 - 26226435
AN - SCOPUS:84949319908
SN - 2667-291X
VL - 138
SP - 349
EP - 355
JO - Cells and Development
JF - Cells and Development
ER -