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Kinked tail mutation results in notochord defects in heterozygotes and distal visceral endoderm defects in homozygotes
Author(s) -
Farkas Deborah R.,
Chapman Deborah L.
Publication year - 2009
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.22141
Subject(s) - biology , endoderm , notochord , anatomy , heterozygote advantage , embryo , phenotype , embryonic stem cell , axial skeleton , zebrafish , embryogenesis , microbiology and biotechnology , genetics , allele , gene
Proper formation of the anterior‐posterior (AP) axis in the developing embryo is critical for the correct patterning and often survival of the organism. In the mouse, an initial step in axis establishment is the specification and migration of the distal visceral endoderm (DVE). We have identified a semi‐dominant spontaneous mutation in mouse, named kinked tail ( knk ), which when heterozygous results in a kinky tail phenotype due to fusions and dysmorphology of the tail vertebrae. Vertebral fusions appear to be a secondary effect of notochord thickening and branching in the tail region. Homozygosity for knk results in early embryonic lethality by embryonic day 8.5 due to improper timing of DVE specification and migration, and subsequent failure to establish the AP axis. Developmental Dynamics 238:3237–3247, 2009. © 2009 Wiley‐Liss, Inc.