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Drosophila jumu modulates apoptosis via a JNK-dependent pathway and is required for other processes in wing development
Previous studies in several model organisms have revealed that members of the Forkhead (Fkh) transcription factor family have multiple functions. Drosophila Jumeau (Jumu), a member of this family, participates in cardiogenesis, hematopoiesis and immune system homeostasis. Here, we show that loss of...
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Published in: | Apoptosis (London) 2019-06, Vol.24 (5-6), p.465-477 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Previous studies in several model organisms have revealed that members of the Forkhead (Fkh) transcription factor family have multiple functions.
Drosophila
Jumeau (Jumu), a member of this family, participates in cardiogenesis, hematopoiesis and immune system homeostasis. Here, we show that loss of
jumu
function positively regulates or triggers apoptosis via a JNK-dependent pathway in wing development.
jumu
mutants showed reduced wing size and increased apoptosis. Moreover, we observed a loss of the anterior cross vein (ACV) phenotype that was similar to that observed in wings in which JNK signaling has been ectopically activated. The JNK signaling markers
puckered
(
puc
) and p-JNK were also significantly increased in the wing discs of
jumu
mutants. In addition, apoptosis induced by the loss of
jumu
was rescued by knocking down JNK, indicating a role for JNK in reducing
jumu
-induced apoptosis. Jumu could also control wing margin development via the positive regulation of
cut
expression, and the observed wing margin defect did not result from a loss of
jumu
-induced apoptosis. Further,
jumu
deficiency in the pupal wing could induce multiple wing hairs via a Rho1-mediated planar cell polarity pathway, but abnormal
Rho1
expression was not why
jumu
loss induced apoptosis via a JNK-dependent pathway in wing discs. |
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ISSN: | 1360-8185 1573-675X |
DOI: | 10.1007/s10495-019-01527-x |