Zachary T Morrow1, Adrienne M Maxwell1, Kazuyuki Hoshijima2, Jared C Talbot1,3,4, David J Grunwald2, Sharon L Amacher1,3,4,5. 1. Department of Molecular Genetics, The Ohio State University, Columbus, Ohio. 2. Department of Human Genetics, University of Utah School of Medicine, Salt Lake City, Utah. 3. Department of Biological Chemistry and Pharmacology, The Ohio State University School of Medicine, Columbus, Ohio. 4. Center for Muscle Health and Neuromuscular Disorders, The Ohio State University and Nationwide Children's Hospital, Columbus, Ohio. 5. Center for RNA Biology, The Ohio State University, Columbus, Ohio.
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.
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 zebrafishtbx6l 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.
Authors: Jared C Talbot; Emily M Teets; Dhanushika Ratnayake; Phan Q Duy; Peter D Currie; Sharon L Amacher Journal: Development Date: 2019-05-15 Impact factor: 6.868
Authors: Daniel P S Osborn; Kuoyu Li; Stephen J Cutty; Andrew C Nelson; Fiona C Wardle; Yaniv Hinits; Simon M Hughes Journal: Development Date: 2020-04-28 Impact factor: 6.862