Roles of the FOXA transcription factor Fork head in autophagic developmental cell death

Cell death during Drosophila melanogaster metamorphosis is controlled by the steroid hormone 20-hydroxyecdysone (20E). Elements of the signaling pathway that triggers death are known, but it is not known why some tissues, and not others, die in response to a particular hormone pulse. We found that loss of the tissue-specific transcription factor Fork head (Fkh) is both required and sufficient to specify a death response to 20E in the larval salivary glands. Loss of fkh itself is a steroid-controlled event that is mediated by the 20E-induced BR-C gene, and that renders the key death regulators hid and reaper hormone responsive. These results implicate the D. melanogaster FOXA orthologue Fkh with a novel function as a competence factor for steroid-controlled cell death. They explain how a specific tissue is singled out for death, and why this tissue survives earlier hormone pulses. More generally, they suggest that cell identity factors like Fkh play a pivotal role in the normal control of developmental cell death.

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Faculty Opinions recommendation of Timing of the onset of a developmental cell death is controlled by transcriptional induction of the C. elegans ced-3 caspase-encoding gene.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1069756.522682 ◽

2007 ◽

Author(s):

Jonathan Hodgkin

Keyword(s):

Cell Death ◽

C Elegans ◽

Encoding Gene ◽

Developmental Cell Death ◽

Transcriptional Induction

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Faculty Opinions recommendation of Alternative pathway of cell death in Drosophila mediated by NF-κB transcription factor Relish.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.13828962.793478950 ◽

2013 ◽

Author(s):

Neal Silverman

Keyword(s):

Cell Death ◽

Transcription Factor ◽

Alternative Pathway

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Faculty Opinions recommendation of miR-14 regulates autophagy during developmental cell death by targeting ip3-kinase 2.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.721801894.793505852 ◽

2015 ◽

Author(s):

Will Wood

Keyword(s):

Cell Death ◽

Developmental Cell Death

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c-junIs Dispensable for Developmental Cell Death and Axogenesis in the Retina

Journal of Neuroscience ◽

10.1523/jneurosci.19-11-04349.1999 ◽

1999 ◽

Vol 19 (11) ◽

pp. 4349-4359 ◽

Cited By ~ 20

Author(s):

Karl-Heinz Herzog ◽

Shu-Cheng Chen ◽

James I. Morgan

Keyword(s):

Cell Death ◽

Developmental Cell Death

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SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis

Scientific Reports ◽

10.1038/s41598-021-91293-1 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Kalyan Mahapatra ◽

Sujit Roy

Keyword(s):

Cell Cycle ◽

Dna Damage ◽

Cell Death ◽

Transcription Factor ◽

Programmed Cell Death ◽

Salinity Stress ◽

Crucial Role ◽

Genome Stability ◽

Cell Cycle Checkpoint ◽

Cell Cycle Regulators

AbstractAs like in mammalian system, the DNA damage responsive cell cycle checkpoint functions play crucial role for maintenance of genome stability in plants through repairing of damages in DNA and induction of programmed cell death or endoreduplication by extensive regulation of progression of cell cycle. ATM and ATR (ATAXIA-TELANGIECTASIA-MUTATED and -RAD3-RELATED) function as sensor kinases and play key role in the transmission of DNA damage signals to the downstream components of cell cycle regulatory network. The plant-specific NAC domain family transcription factor SOG1 (SUPPRESSOR OF GAMMA RESPONSE 1) plays crucial role in transducing signals from both ATM and ATR in presence of double strand breaks (DSBs) in the genome and found to play crucial role in the regulation of key genes involved in cell cycle progression, DNA damage repair, endoreduplication and programmed cell death. Here we report that Arabidopsis exposed to high salinity shows generation of oxidative stress induced DSBs along with the concomitant induction of endoreduplication, displaying increased cell size and DNA ploidy level without any change in chromosome number. These responses were significantly prominent in SOG1 overexpression line than wild-type Arabidopsis, while sog1 mutant lines showed much compromised induction of endoreduplication under salinity stress. We have found that both ATM-SOG1 and ATR-SOG1 pathways are involved in the salinity mediated induction of endoreduplication. SOG1was found to promote G2-M phase arrest in Arabidopsis under salinity stress by downregulating the expression of the key cell cycle regulators, including CDKB1;1, CDKB2;1, and CYCB1;1, while upregulating the expression of WEE1 kinase, CCS52A and E2Fa, which act as important regulators for induction of endoreduplication. Our results suggest that Arabidopsis undergoes endoreduplicative cycle in response to salinity induced DSBs, showcasing an adaptive response in plants under salinity stress.

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Suppression of E1A-Mediated Transformation by the p50E4F Transcription Factor

Molecular and Cellular Biology ◽

10.1128/mcb.19.7.4739 ◽

1999 ◽

Vol 19 (7) ◽

pp. 4739-4749 ◽

Cited By ~ 7

Author(s):

Elma R. Fernandes ◽

Robert J. Rooney

Keyword(s):

Cell Death ◽

Transcription Factor ◽

Suppressive Effect ◽

Culture Conditions ◽

Binding Activity ◽

Cellular Transcription Factor ◽

Dna Binding Activity ◽

3T3 Fibroblasts ◽

Induced Apoptosis ◽

Nih 3T3

ABSTRACT The adenovirus E1A gene can act as an oncogene or a tumor suppressor, with the latter effect generally arising from the induction of apoptosis or the repression of genes that provide oncogenic growth stimuli (e.g., HER-2/c-erbB2/neu) or increased metastatic invasiveness (e.g., metalloproteases). In this study, coexpression of E1A and p50E4F, a cellular transcription factor whose DNA binding activity is stimulated by E1A, suppressed colony formation by NIH 3T3 cells and transformation of primary rat embryo fibroblasts but had no observed effect in the absence of E1A. Domains in p50E4F required for stimulation of the adenovirus E4 promoter were required for the suppressive effect, indicating a transcriptional mechanism. In serum-containing media, retroviral expression of p50E4F in E1A13S/ras-transformed NIH 3T3 fibroblasts had little effect on subconfluent cultures but accelerated a decline in viability after the cultures reached confluence. Cell death occurred by both apoptosis and necrosis, with the predominance of each process determined by culture conditions. In serum-free media, p50E4F accelerated E1A-induced apoptosis. The results suggest that p50E4F sensitizes cells to signals or conditions that cause cell death.

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