Modulation of quail intestinal and egg shell gland calbindin ( Mr 28,000) gene expression by vitamin D 3, 1,25-dihydroxyvitamin D 3 and egg laying

Abstract

The effects of vitamin D 3 sources, egg production and egg cycle on the genomic expression of calbindin (M r 28,000) in the intestine and egg shell gland (ESG) of quail were characterized by Northern blot and solution hybridization, using synthetic oligonucleotide probe. In vitamin D 3- or 1,25-dihydroxyvitamin D 3 (1,25-(OH) 2D 3)-fed quail, onset of egg production induced duodenal and ESG calbindin mRNA and calbindin synthesis. Duodenal calbindin mRNA was slightly higher during the period of shell calcification as compared with the period during which shells were not formed (ESG inactivity). ESG calbindin mRNA was markedly higher during the period of shell calcification than of ESG inactivity. Increasing dietary intake of [ 3H]1α-hydroxyvitamin D 3 increased the duodenal, but not ESG, content of 1,25-(OH) 2D 3 and calbindin. Duodenal calbindin and its mRNA were absent in vitamin D-deficient quail and were not affected by egg laying. ESG calbindin in the vitamin D-deficient quail was not affected by egg laying, but calbindin mRNA increased in the vitamin D-deficient birds during shell calcification. The results suggest that: (a) intestinal calbindin mRNA and calbindin are induced and/or regulated, either directly or indirectly, by 1,25-(OH) 2D 3; (b) intestinal calbindin and its mRNA are further induced at the onset of egg laying by an additional stimulator besides 1,25-(OH) 2D 3; (c) 1,25-(OH) 2D 3 is required for the expression of the latter stimulator; (d) ESG calbindin mRNA and calbindin are induced in egg-laying birds by a stimulator associated with the egg cycle; and (e) the induction of ESG calbindin mRNA does not need vitamin D metabolites, but 1,25-(OH) 2D 3 is required for the translation of the mRNA.