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Genesis. 2013 Mar;51(3):147-62. doi: 10.1002/dvg.22354. Epub 2012 Nov 20.

Regulating cell morphogenesis: the Drosophila Jun N-terminal kinase pathway.

Author information

1
Developmental Neurobioloy and Neurophysiology Department, Instituto de Neurobiología, Universidad Nacional Autónoma de México, Boulevard Juriquilla #3001, Querétaro, Querétaro, México, c.p. 76230.

Abstract

The Jun-N-terminal Kinase pathway (JNK), known also as stress activated protein kinase pathway (SAPK), is an eukaryotic evolutionarily conserved signaling pathway. From a purported evolutionarily "ancient" function as stress mediator, it evolved in multicellular eukaryotes to permanent roles in development, without leaving its original function. In Drosophila melanogaster, it is required for follicle cell morphogenesis, embryonic dorsal closure, pupal thoracic closure and genital disc rotation closure, all processes with requisite cell shape changes. Besides, it is activated during wound healing and in response to stress (UV irradiation, oxidative stress) where it may signal cell death or proliferation. Despite these varied roles, it has a conserved core of molecules that follow the MAPKKK/MAPKK/MAPK logic of mitogen activated protein kinases pathways. Regulation of the JNK pathway appears majorly negative, with phosphatases, transcription factors and proteins of novel structure "holding back" on JNK activation in different tissues. This particular mode of regulation may hark back to the pathway's origin as stress detector and responder, implying readiness to respond, from which the developmental roles may have evolved as conditions demanding obligate and predicted stress responses (i.e., embryonic dorsal closure viewed as a "wound of development").

PMID:
23109363
DOI:
10.1002/dvg.22354
[Indexed for MEDLINE]

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