Tbx6l and tbx16 are redundantly required for posterior paraxial mesoderm formation during zebrafish embryogenesis. Issue 10 (30th August 2017)

• Record Type: Journal Article
• Authors: Morrow, Zachary T.; Maxwell, Adrienne M.; Hoshijima, Kazuyuki; Talbot, Jared C.; Grunwald, David J.; Amacher, Sharon L.
• Is Part Of: Developmental dynamics. Volume 246:Issue 10(2017)
• Page Start: 759
• Page End: 769
• Publication Date: 2017-08-30
• Subjects: T‐box genes -- spadetail -- ntl/Brachyury -- fss/tbx6 -- mesogenin -- somitogenesis; Morphogenesis -- Periodicals; Anatomy -- Periodicals; Anatomie -- Périodiques; Biologie du développement -- Périodiques; 571.833
• DOI: 10.1002/dvdy.24547
• Languages: English
• ISSNs: 1058-8388

Abstract

Abstract : Background: T‐box genes encode a large transcription factor family implicated in many aspects of development. We are focusing on two related zebrafish T‐box genes, tbx6l and tbx16, that are expressed in highly overlapping patterns in embryonic paraxial mesoderm. tbx16 mutants are deficient in trunk, but not tail, somites; we explored whether presence of tail somites in tbx16 mutants was due to compensatory function provided by the tbx6l gene.Results: We generated two zebrafish tbx6l mutant alleles. Loss of tbx6l has no apparent effect on embryonic development, nor does tbx6l loss enhance the phenotype of two other T‐box gene mutants, ta and tbx6, or of the mesp family gene mutant msgn1 . In contrast, loss of tbx6l function dramatically enhances the paraxial mesoderm deficiency of tbx16 mutants.Conclusions: These data demonstrate that tbx6l and tbx16 genes function redundantly to direct tail somite development. tbx6l single mutants develop normally because tbx16 fully compensates for loss of tbx6l function. However, tbx6l only partially compensates for loss of tbx16 function. These results resolve the question of why loss of function of tbx16 gene, which is expressed throughout the ventral and paraxial mesoderm, profoundly affects somite development in the trunk but not the tail. Developmental Dynamics 246:759–769, 2017 . © 2017 Wiley Periodicals, Inc. Key Findings: Loss of zebrafish tbx6l alone has little to no effect on embryonic development because tbx16, a closely related gene, compensates for loss of tbx6l function. Loss of tbx6l enhances the tbx16 mutant phenotype, revealing that tbx6l functions redundantly with tbx16 during tail paraxial mesoderm development. Double mutant analyses reveal that tbx6l does not appear to genetically interact with ta or tbx6, two other mesodermally‐expressed T‐box genes. In addition, tbx6l loss does not enhance the supernumerary somite phenotype of mesogenin1 mutants.