Abstract:
:Epithelial sheet movement is an essential morphogenetic process during mouse embryonic eyelid closure in which Mitogen-Activated Protein 3 Kinase 1 (MAP3K1) and c-Jun play a critical role. Here we show that MAP3K1 associates with the cytoskeleton, activates Jun N-terminal kinase (JNK) and actin polymerization, and promotes the eyelid inferior epithelial cell elongation and epithelium protrusion. Following epithelium protrusion, c-Jun begins to express and acts to promote ERK phosphorylation and migration of the protruding epithelial cells. Homozygous deletion of either gene causes defective eyelid closure, but non-allelic non-complementation does not occur between Map3k1 and c-Jun and the double heterozygotes have normal eyelid closure. Results from this study suggest that MAP3K1 and c-Jun signal through distinct temporal-spatial pathways and that productive epithelium movement for eyelid closure requires the consecutive action of MAP3K1-dependent cytoskeleton reorganization followed by c-Jun-mediated migration.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Meng Q,Mongan M,Wang J,Tang X,Zhang J,Kao W,Xia Ydoi
10.1016/j.ydbio.2014.09.001subject
Has Abstractpub_date
2014-11-01 00:00:00pages
29-37issue
1eissn
0012-1606issn
1095-564Xpii
S0012-1606(14)00443-6journal_volume
395pub_type
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