JNK signaling coordinates integrin and actin functions during Drosophila embryogenesis.
Epithelial movements are key morphogenetic events in animal development. They are driven by multiple mechanisms, including signal-dependent changes in cytoskeletal organization and in cell adhesion. Such processes must be controlled precisely and coordinated to accurately sculpt the three-dimensional form of the developing organism. By observing the Drosophila epidermis during embryonic development using confocal time-lapse microscopy, we have investigated how signaling through the Jun-N-terminal kinase (JNK) pathway governs the tissue sheet movements that result in dorsal closure (DC). We find that JNK controls the polymerization of actin into a cable at the epidermal leading edge as previously suggested, as well as the joining (zipping) of the contralateral epithelial cell sheets. Here, we show that zipping is mediated by regulation of the integrins myospheroid and scab. Our data demonstrate that JNK signaling regulates a set of target genes that cooperate to facilitate epithelial movement and closure.
Homsy
Jason G
JG
Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, New York 14642, USA.
Jasper
Heinrich
H
Peralta
Xomalin G
XG
Wu
Hai
H
Kiehart
Daniel P
DP
Bohmann
Dirk
D
D000199:Actins / Q000378:metabolism*; D000818:Animals; D004331:Drosophila melanogaster / Q000196:embryology* / Q000235:genetics / Q000378:metabolism*; D047108:Embryonic Development; D018507:Gene Expression Regulation, Developmental; D016023:Integrins / Q000378:metabolism*; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D015398:Signal Transduction
D000199:Actins; D016023:Integrins; D048031:JNK Mitogen-Activated Protein Kinases