Mutations affecting somite formation and patterning in the zebrafish, Danio rerio

Van Eeden F, Granato M, Schach U, Brand M, Furutani Seiki M, Haffter P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R, Mullins M, Odenthal J, Warga R, Allende M, Weinberg E, Nüsslein Volhard C. 1996. Mutations affecting somite formation and patterning in the zebrafish, Danio rerio. Development. 123(1), 153–164.


Journal Article | Published | English

Scopus indexed
Author
Van Eeden, Fredericus; Granato, Michael; Schach, Ursula; Brand, Michael; Furutani Seiki, Makoto; Haffter, Pascal; Hammerschmidt, Matthias; Heisenberg, Carl-Philipp ISTA ; Jiang, Yunjin; Kane, Donald; Kelsh, Robert; Mullins, Mary
All
Abstract
Somitogenesis is the basis of segmentation of the mesoderm in the trunk and tail of vertebrate embryos, Two groups of mutants with defects in this patterning process have been isolated in our screen for zygotic mutations affecting the embryonic development of the zebrafish (Danio rerio), In mutants of the first group, boundaries between individual somites are invisible early on, although the paraxial mesoderm is present, Later, irregular boundaries between somites are present, Mutations infused somites (fss) and beamter (bea) affect all somites, whereas mutations in deadly seven (des), after eight (aei) and white tail (wit) only affect the more posterior somites, Mutants of all genes but wit are homozygous viable and fertile, Skeletal stainings and the expression pattern of myoD and snail1 suggest that anteroposterior patterning within individual somites is abnormal, In the second group of mutants, formation of the horizontal myoseptum, which separates the dorsal and ventral part of the myotome, is reduced, Six genes have been defined in this group (you-type genes), yea-too mutants show the most severe phenotype; in these the adaxial cells, muscle pioneers and the primary motoneurons are affected, in addition to the horizontal myoseptum. The horizontal myoseptum is also missing in mutants that lack a notochord. The similarity of the somite phenotype in mutants lacking the notochord and in the you-type mutants suggests that the genes mutated in these two groups are involved in a signaling pathway from the notochord, important for patterning of the somites.
Publishing Year
Date Published
1996-12-01
Journal Title
Development
Acknowledgement
We would like to thank P. Ingham and T. Whitfield for valuable comments on the manuscript and cDNA probes, S. Schulte-Merker for the Ntl antibody and J. Eisen and R. BreMiller for the znp-1 antibody.
Volume
123
Issue
1
Page
153 - 164
ISSN
IST-REx-ID

Cite this

Van Eeden F, Granato M, Schach U, et al. Mutations affecting somite formation and patterning in the zebrafish, Danio rerio. Development. 1996;123(1):153-164. doi:10.1242/dev.123.1.153
Van Eeden, F., Granato, M., Schach, U., Brand, M., Furutani Seiki, M., Haffter, P., … Nüsslein Volhard, C. (1996). Mutations affecting somite formation and patterning in the zebrafish, Danio rerio. Development. Company of Biologists. https://doi.org/10.1242/dev.123.1.153
Van Eeden, Fredericus, Michael Granato, Ursula Schach, Michael Brand, Makoto Furutani Seiki, Pascal Haffter, Matthias Hammerschmidt, et al. “Mutations Affecting Somite Formation and Patterning in the Zebrafish, Danio Rerio.” Development. Company of Biologists, 1996. https://doi.org/10.1242/dev.123.1.153.
F. Van Eeden et al., “Mutations affecting somite formation and patterning in the zebrafish, Danio rerio,” Development, vol. 123, no. 1. Company of Biologists, pp. 153–164, 1996.
Van Eeden F, Granato M, Schach U, Brand M, Furutani Seiki M, Haffter P, Hammerschmidt M, Heisenberg C-PJ, Jiang Y, Kane D, Kelsh R, Mullins M, Odenthal J, Warga R, Allende M, Weinberg E, Nüsslein Volhard C. 1996. Mutations affecting somite formation and patterning in the zebrafish, Danio rerio. Development. 123(1), 153–164.
Van Eeden, Fredericus, et al. “Mutations Affecting Somite Formation and Patterning in the Zebrafish, Danio Rerio.” Development, vol. 123, no. 1, Company of Biologists, 1996, pp. 153–64, doi:10.1242/dev.123.1.153.
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