Literature DB >> 17464325

The Drosophila caspases Strica and Dronc function redundantly in programmed cell death during oogenesis.

J S Baum1, E Arama, H Steller, K McCall.   

Abstract

Programmed cell death (PCD) in the Drosophila ovary occurs either during mid-oogenesis, resulting in degeneration of the entire egg chamber or during late oogenesis, to facilitate the development of the oocyte. PCD during oogenesis is regulated by mechanisms different from those that control cell death in other Drosophila tissues. We have analyzed the role of caspases in PCD of the female germline by examining caspase mutants and overexpressing caspase inhibitors. Imprecise P-element excision was used to generate mutants of the initiator caspase strica. While null mutants of strica or another initiator caspase, dronc, display no ovary phenotype, we find that strica exhibits redundancy with dronc, during both mid- and late oogenesis. Ovaries of double mutants contain defective mid-stage egg chambers similar to those reported previously in dcp-1 mutants, and mature egg chambers with persisting nurse cell nuclei. In addition, the effector caspases drice and dcp-1 also display redundant functions during late oogenesis, resulting in persisting nurse cell nuclei. These findings indicate that caspases are required for nurse cell death during mid-oogenesis, and participate in developmental nurse cell death during late oogenesis. This reveals a novel pathway of cell death in the ovary that utilizes strica, dronc, dcp-1 and drice, and importantly illustrates strong redundancy among the caspases.

Entities:  

Mesh:

Substances:

Year:  2007        PMID: 17464325     DOI: 10.1038/sj.cdd.4402155

Source DB:  PubMed          Journal:  Cell Death Differ        ISSN: 1350-9047            Impact factor:   15.828


  39 in total

1.  Physiological apoptosis of polar cells during Drosophila oogenesis is mediated by Hid-dependent regulation of Diap1.

Authors:  A Khammari; F Agnès; P Gandille; A-M Pret
Journal:  Cell Death Differ       Date:  2010-11-26       Impact factor: 15.828

2.  p53-independent apoptosis limits DNA damage-induced aneuploidy.

Authors:  Laura M McNamee; Michael H Brodsky
Journal:  Genetics       Date:  2009-04-13       Impact factor: 4.562

Review 3.  Novel roles of apoptotic caspases in tumor repopulation, epigenetic reprogramming, carcinogenesis, and beyond.

Authors:  Ruya Zhao; Rayan Kaakati; Andrew K Lee; Xinjian Liu; Fang Li; Chuan-Yuan Li
Journal:  Cancer Metastasis Rev       Date:  2018-09       Impact factor: 9.264

Review 4.  Non-apoptotic cell death in animal development.

Authors:  Lena M Kutscher; Shai Shaham
Journal:  Cell Death Differ       Date:  2017-02-17       Impact factor: 15.828

5.  The caspase-8 homolog Dredd cleaves Imd and Relish but is not inhibited by p35.

Authors:  Chan-Hee Kim; Donggi Paik; Florentina Rus; Neal Silverman
Journal:  J Biol Chem       Date:  2014-06-02       Impact factor: 5.157

6.  Control of non-apoptotic nurse cell death by engulfment genes in Drosophila.

Authors:  Allison K Timmons; Albert A Mondragon; Tracy L Meehan; Kimberly McCall
Journal:  Fly (Austin)       Date:  2016-09-29       Impact factor: 2.160

Review 7.  Genetic control of programmed cell death (apoptosis) in Drosophila.

Authors:  Dongbin Xu; Sarah E Woodfield; Tom V Lee; Yun Fan; Christian Antonio; Andreas Bergmann
Journal:  Fly (Austin)       Date:  2009-01-08       Impact factor: 2.160

Review 8.  Cracking open cell death in the Drosophila ovary.

Authors:  Tracy L Pritchett; Elizabeth A Tanner; Kimberly McCall
Journal:  Apoptosis       Date:  2009-08       Impact factor: 4.677

Review 9.  Diversity of cell death pathways: insight from the fly ovary.

Authors:  Victoria K Jenkins; Allison K Timmons; Kimberly McCall
Journal:  Trends Cell Biol       Date:  2013-08-19       Impact factor: 20.808

10.  The cleaved-Caspase-3 antibody is a marker of Caspase-9-like DRONC activity in Drosophila.

Authors:  Y Fan; A Bergmann
Journal:  Cell Death Differ       Date:  2009-12-04       Impact factor: 15.828

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.