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Regulation of Five Tubulin Isotypes by Thyroid Hormone During Brain Development
Author(s) -
Aniello Francesco,
Couchie Dominique,
Gripois Daniel,
Nunez Jacques
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb06381.x
Subject(s) - tubulin , thyroid , hormone , endocrinology , biology , brain development , neuroscience , medicine , microtubule , microbiology and biotechnology
: Nucleic acid probes derived from the 3’noncoding region of five tubulin cDNAs were used to study the effects of thyroid hormone deficiency on the expression of the mRNAs encoding two α (α 1 and α 2 )‐and three β (β 2 , β 4 , and β 5 )‐tubulin isotypes in the developing cerebral hemispheres and cerebellum. The content of α 1 , which markedly declines during development in both brain regions, is maintained at high levels in the hypothyroid cerebellum, whereas it is decreased in the cerebral hemispheres. The α 2 level also declines during development and is decreased in both regions by thyroid hormone deficiency, but only during the two first postnatal weeks. Thyroid hormone deficiency slightly increases at all stages the β 2 level in the cerebellum, whereas a decrease is observed at early stages in the cerebral hemispheres. The ft level seems to be independent of thyroid hormone in the cerebral hemispheres, whereas it decreases at early stages in the hypothyroid cerebellum. Finally, the expression of the brain‐specific β 4 isotype is markedly depressed by thyroid hormone deficiency, particularly in the cerebellum. These data suggest that the genes encoding the tubulin isotypes are, directly or not, differently regulated by thyroid hormone during brain development This might contribute to abnormal neurite outgrowth seen in the hypothyroid brain and therefore to impairment in brain functions produced by thyroid hormone deficiency.