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Requirement for commissureless2 function during dipteran insect nerve cord development
Author(s) -
Sarro Joseph,
Andrews Emily,
Sun Longhua,
Behura Susanta K.,
Tan John C.,
Zeng Erliang,
Severson David W.,
DumanScheel Molly
Publication year - 2013
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.24059
Subject(s) - biology , ventral nerve cord , drosophila melanogaster , commissure , insect , anatomy , aedes aegypti , melanogaster , phenocopy , vector (molecular biology) , gene , phenotype , neuroscience , nervous system , larva , genetics , botany , recombinant dna
Background: In Drosophila melanogaster , commissureless ( comm ) function is required for proper nerve cord development. Although comm orthologs have not been identified outside of Drosophila species, some insects possess orthologs of Drosophila comm2 , which may also regulate embryonic nerve cord development. Here, this hypothesis is explored through characterization of comm2 genes in two disease vector mosquitoes. Results: Culex quinquefasciatus (West Nile and lymphatic filiariasis vector) has three comm2 genes that are expressed in the developing nerve cord. Aedes aegypti (dengue and yellow fever vector) has a single comm2 gene that is expressed in commissural neurons projecting axons toward the midline. Loss of comm2 function in both A. aegypti and D. melanogaster was found to result in loss of commissure defects that phenocopy the frazzled ( fra ) loss of function phenotypes observed in both species. Loss of fra function in either insect was found to result in decreased comm2 transcript levels during nerve cord development. Conclusions: The results of this investigation suggest that Fra down‐regulates repulsion in precrossing commissural axons by regulating comm2 levels in both A. aegypti and D. melanogaster , both of which require Comm2 function for proper nerve cord development. Developmental Dynamics 242:1466–1477, 2013 . © 2013 Wiley Periodicals, Inc.