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Tuba1a gene expression is regulated by KLF6/7 and is necessary for CNS development and regeneration in zebrafish. Mol Cell Neurosci 2010 Apr;43(4):370-83

Date

02/04/2010

Pubmed ID

20123021

Pubmed Central ID

PMC2837137

DOI

10.1016/j.mcn.2010.01.004

Scopus ID

2-s2.0-77649269805 (requires institutional sign-in at Scopus site)   52 Citations

Abstract

We report that knockdown of the alpha1 tubulin isoform Tuba1a, but not the highly related Tuba1b, dramatically impedes nervous system formation during development and RGC axon regeneration following optic nerve injury in adults. Within the tuba1a promoter, a G/C-rich element was identified that is necessary for tuba1a induction during RGC differentiation and optic axon regeneration. KLF6a and 7a, which we previously reported are essential for optic axon regeneration (Veldman et al., 2007), bind this G/C-rich element and transactivate the tuba1a promoter. In vivo knockdown of KLF6a and 7a attenuate regeneration-dependent activation of the endogenous tuba1a and p27 genes. These results suggest tuba1a expression is necessary for CNS development and regeneration and that KLF6a and 7a mediate their effects, at least in part, via transcriptional control of tuba1a promoter activity.

Author List

Veldman MB, Bemben MA, Goldman D

Author

Matthew B. Veldman PhD Assistant Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Animals, Genetically Modified
Electrophoretic Mobility Shift Assay
Gene Expression Regulation
Immunohistochemistry
In Situ Hybridization
Nerve Regeneration
Nerve Tissue Proteins
Optic Nerve Injuries
Promoter Regions, Genetic
RNA, Messenger
Retina
Reverse Transcriptase Polymerase Chain Reaction
Tubulin
Zebrafish
Zebrafish Proteins