ZFIN ID: ZDB-PUB-010705-5
Functional repression of islet-2 by disruption of complex with Ldb impairs peripheral axonal outgrowth in embryonic zebrafish
Segawa, H., Miyashita, T., Hirate, Y., Higashijima, S., Chino, N., Uyemura, K., Kikuchi, Y., and Okamoto, H.
Date: 2001
Source: Neuron 30(2): 423-436 (Journal)
Registered Authors: Higashijima, Shin-ichi, Hirate, Yoshikazu, Kikuchi, Yutaka, Miyashita, Toshio, Okamoto, Hitoshi, Segawa, Hiroshi
Keywords: none
MeSH Terms: Animals; Axons/physiology*; Binding Sites; Embryo, Nonmammalian/physiology; Genes, Reporter (all 24) expand
PubMed: 11395004 Full text @ Neuron
ABSTRACT
Islet-2 is a LIM/homeodomain-type transcription factor of the Islet-1 family expressed in embryonic zebrafish. Two Islet-2 molecules bind to the LIM domain binding protein (Ldb) dimers. Overexpression of the LIM domains of Islet-2 or the LIM-interacting domain of Ldb proteins prevented binding of Islet-2 to Ldb proteins in vitro and caused similar in vivo defects in positioning, peripheral axonal outgrowth, and neurotransmitter expression by the Islet-2-positive primary sensory and motor neurons as the defects induced by injection of Islet-2-specific antisense morpholino oligonucleotide. These and other experiments, i.e., mosaic analysis, coexpression of full-length Islet-2, and overexpression of the chimeric LIM domains derived from two different Islet-1 family members, demonstrated that Islet-2 regulates neuronal differentiation by forming a complex with Ldb dimers and possibly with some other Islet-2-specific cofactors.
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