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Developmental regulation and expression of the zebrafish connexin43 gene
Author(s) -
Chatterjee Bishwanath,
Chin Alvin J.,
Valdimarsson Gunnar,
Finis Carla,
Sonntag Jennifer M.,
Choi Bo Yon,
Tao Liang,
Balasubramanian Krithika,
Bell Carolyn,
Krufka Alison,
Kozlowski David J.,
Johnson Ross G.,
Lo Cecilia W.
Publication year - 2005
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.20426
Subject(s) - biology , zebrafish , danio , notochord , gene , conserved sequence , gastrulation , genetics , maternal to zygotic transition , transcription factor , gene expression , in situ hybridization , microbiology and biotechnology , peptide sequence , embryogenesis , zygote
We cloned and sequenced the zebrafish ( Danio rerio ) connexin43 (Cx43α1) gene. The predicted protein sequence shows a high degree of sequence conservation. Transcript analyses revealed multiple transcription start sites and a potential alternative transcript encoding a N‐terminally truncated Cx43α1 protein. Maternal Cx43α1 transcripts were detected, with zygotic expression initiated before gastrulation. In situ hybridization revealed many Cx43α1 expression domains, including the notochord and brain, heart and vasculature, many resembling patterns seen in mammalian embryos. Of interest, a reporter construct under control of the mouse Cx43α1 promoter was observed to drive green fluorescent protein expression in zebrafish embryos in domains mimicking the native Cx43α1 expression pattern in fish and mice. Sequence comparison between the mouse and zebrafish Cx43α1 promoter sequences showed the conservation of several transcription factor motifs, which otherwise shared little overall sequence homology. The conservation of protein sequence and developmental gene regulation would suggest that Cx43α1 gap junctions are likely to have conserved roles in vertebrate embryonic development. Developmental Dynamics 233:890–906, 2005. © 2005 Wiley‐Liss, Inc.