TY - JOUR
T1 - Differential requirements for COPI transport during vertebrate early development
AU - Coutinho, Pedro
AU - Parsons, Michael J.
AU - Thomas, Kevin A.
AU - Hirst, Elizabeth M.A.
AU - Saúde, Leonor
AU - Campos, Isabel
AU - Williams, P. Huw
AU - Stemple, Derek L.
N1 - Funding Information:
We thank Jean-Paul Vincent, Jonathan Millar, Alex Gould, Ben Feldman, Stuart Smith, James Briscoe, Mike Sargent, Gavin Wright, and Chris Schoenherr for helpful discussions and comments on the manuscript. M.J.P., K.A.T., E.M.A.H., and D.L.S. were supported by the Medical Research Council, United Kingdom. P.C. and L.S. were supported by PhD studentships from Fundação para a Ciência e Tecnologia, Programa PRAXIS XXI (Portugal). I.C. was funded by the Programa Gulbenkian de Doutoramento em Biologia e Medicina and Programa PRAXIS XXI (Portugal). The authors also acknowledge the support of the Wellcome Trust.
PY - 2004/10
Y1 - 2004/10
N2 - The coatomer vesicular coat complex is essential for normal Golgi and secretory activities in eukaryotic cells. Through positional cloning of genes controlling zebrafish notochord development, we found that the sneezy, happy, and dopey loci encode the α, β, and β′ subunits of the coatomer complex. Export from mutant endoplasmic reticulum is blocked, Golgi structure is disrupted, and mutant embryos eventually degenerate due to widespread apoptosis. The early embryonic phenotype, however, demonstrates that despite its "housekeeping" functions, coatomer activity is specifically and cell autonomously required for normal chordamesoderm differentiation, perinotochordal basement membrane formation, and melanophore pigmentation. Hence, differential requirements for coatomer activity among embryonic tissues lead to tissue-specific developmental defects. Moreover, we note that the mRNA encoding α coatomer is strikingly upregulated in notochord progenitors, and we present data suggesting that α coatomer transcription is tuned to activity- and cell type-specific secretory loads.
AB - The coatomer vesicular coat complex is essential for normal Golgi and secretory activities in eukaryotic cells. Through positional cloning of genes controlling zebrafish notochord development, we found that the sneezy, happy, and dopey loci encode the α, β, and β′ subunits of the coatomer complex. Export from mutant endoplasmic reticulum is blocked, Golgi structure is disrupted, and mutant embryos eventually degenerate due to widespread apoptosis. The early embryonic phenotype, however, demonstrates that despite its "housekeeping" functions, coatomer activity is specifically and cell autonomously required for normal chordamesoderm differentiation, perinotochordal basement membrane formation, and melanophore pigmentation. Hence, differential requirements for coatomer activity among embryonic tissues lead to tissue-specific developmental defects. Moreover, we note that the mRNA encoding α coatomer is strikingly upregulated in notochord progenitors, and we present data suggesting that α coatomer transcription is tuned to activity- and cell type-specific secretory loads.
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U2 - 10.1016/j.devcel.2004.07.020
DO - 10.1016/j.devcel.2004.07.020
M3 - Article
C2 - 15469843
AN - SCOPUS:5044251197
SN - 1534-5807
VL - 7
SP - 547
EP - 558
JO - Developmental Cell
JF - Developmental Cell
IS - 4
ER -