Abstract:
:Drosophila nemo (nmo) and other Nemo-like kinase family members (Nlks) are well-established key regulators of numerous conserved signaling pathways, such as Wg and BMP. nmo mutants display pleiotropic defects at different developmental stages, including the embryo. In this study we describe a detailed characterization of embryonic cuticle patterning defects associated with maternal loss of nmo. nmo mutant embryos consistently show segmentation defects, most frequently fusions of pairs of denticle belts in alternating segments. These phenotypes are reminiscent of those associated with defects in pair-rule patterning. Genetic interaction studies demonstrate that Nmo promotes Even-skipped (Eve) activity and is required to promote the expression of the Eve target, engrailed (en), in even numbered parasegments. We find that Nmo regulates a subset of Eve activities by stimulating Eve-mediated suppression of the odd-skipped (odd) repressor. Furthermore, we isolate Nmo in a protein complex with Eve and show that Nmo phosphorylates Eve in in vitro kinase assays. These studies reveal a novel role for the Nmo kinase in embryonic pattern formation through its regulation of the homeodomain-containing transcription factor Eve.
journal_name
Dev Bioljournal_title
Developmental biologyauthors
Braid LR,Lee W,Uetrecht AC,Swarup S,Papaianni G,Heiler A,Verheyen EMdoi
10.1016/j.ydbio.2010.04.008subject
Has Abstractpub_date
2010-07-01 00:00:00pages
178-89issue
1-2eissn
0012-1606issn
1095-564Xpii
S0012-1606(10)00238-1journal_volume
343pub_type
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