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The POU transcription factor UNC‐86 controls the timing and ventral guidance of Caenorhabditis elegans axon growth
Author(s) -
OlssonCarter Katherine,
Slack Frank J.
Publication year - 2011
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.22667
Subject(s) - biology , pou domain , axon , caenorhabditis elegans , axon guidance , transcription factor , neuroscience , microbiology and biotechnology , loss function , mutant , anatomy , phenotype , genetics , gene , homeobox
The in vivo mechanisms that coordinate the timing of axon growth and guidance are not well understood. In the Caenorhabditis elegans hermaphrodite specific neurons (HSNs), the lin‐4 microRNA controls the stage of axon initiation independent of the UNC‐40 and SAX‐3 ventral guidance receptors. lin‐4 loss‐of‐function mutants exhibit marked delays in axon outgrowth, while lin‐4 overexpression leads to precocious growth in the L3 larval stage. Here, we show that loss of the POU transcription factor UNC‐86 not only results in penetrant ventral axon growth defects in in the HSNs, but also causes processes to extend in the L1, three stages earlier than wild‐type. This temporal shift is not dependent on UNC‐40 or SAX‐3, and does not require the presence of lin‐4 . We propose that unc‐86(lf ) HSN axons are misguided due to the temporal decoupling of axon initiation and ventral guidance responses. Developmental Dynamics 240:1815–1825, 2011. © 2011 Wiley‐Liss, Inc.