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Volume 272, Number 50, Issue of December 12, 1997 pp. 31738-31746

Cig30, a Mouse Member of a Novel Membrane Protein Gene Family, Is Involved in the Recruitment of Brown Adipose Tissue

(Received for publication, July 2, 1997, and in revised form, August 27, 1997)

Petr Tvrdik , Abolfazl Asadi , Leslie P. Kozak ^¶ , Jan Nedergaard , Barbara Cannon and Anders Jacobsson

From  The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, S-106 91 Stockholm, Sweden and ^¶ The Jackson Laboratory, Bar Harbor, Maine 04609

We have identified a previously uncharacterized gene that is implicated in the thermogenic function of brown adipose tissue of mice. This gene, termed Cig30, is the first mammalian member of a novel gene family comprising several nematode and yeast genes, such as SUR4 and FEN1, mutation of which is associated with highly pleiotropic phenotypes. It codes for a 30-kDa plasma membrane glycoprotein with five putative transmembrane domains. The Cig30 mRNA was readily detected only in brown fat and liver. When animals were exposed to a 3-day cold stress, the Cig30 expression was selectively elevated in brown fat more than 200-fold. Similar increases were brought about in two other conditions of brown fat recruitment, namely during perinatal development and after cafeteria diet. The magnitude of Cig30 mRNA induction in the cold could be mimicked by chronic norepinephrine treatment in vivo. However, in primary cultures of brown adipocytes, a synergistic action of norepinephrine and dexamethasone was required for full expression of the gene, indicating that both catecholamines and glucocorticoids are required for the induction of Cig30. We propose that the CIG30 protein is involved in a pathway connected with brown fat hyperplasia.

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