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Analysis of haploid development based on expression patterns of developmental genes in the medaka Oryzias latipes.

Authors :
Araki, Kazuo
Okamoto, Hiroyuki
Graveson, Ann C.
Nakayama, Ichiro
Nagoya, Hiroyuki
Source :
Development, Growth & Differentiation; Oct2001, Vol. 43 Issue 5, p591-599, 9p, 5 Black and White Photographs, 1 Diagram
Publication Year :
2001

Abstract

The abnormalities of haploid medaka embryos were characterized by comparative analysis of histologic sections and expression patterns of some developmental marker genes between haploids and diploids to clarify whether medaka haploids are useful for identifying mutants. During gastrulation, an obvious defect was first observed as a delay of epiboly and involution. This delay was shown to be caused not by the perturbation of mesoderm induction, but by widespread cell death and disorganization of cell arrangement in the blastoderm. This disorganization of cell arrangement was also detected in various organs, such as the brain, somite and notochord, at a late developmental stage. Ten days after fertilization, a small head and a short body axis were formed; these changes were also observed in haploid embryos in other species, but their cause is unknown. Based on the expression patterns of HNF3β and goosecoid, it was demonstrated that a short and impotent prechordal plate induced near the marginal zone in haploid embryos was responsible for this defect. However, in these experiments it was also demonstrated that many major organs in haploids, such as the somite and notochord, differentiated incompletely but were present. Therefore, it was concluded that haploid screening is suitable for identifying mutations revealed by an obvious phenotype, such as dorsoventral polarity. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00121592
Volume :
43
Issue :
5
Database :
Complementary Index
Journal :
Development, Growth & Differentiation
Publication Type :
Academic Journal
Accession number :
5251596
Full Text :
https://doi.org/10.1046/j.1440-169X.2001.00601.x