Why the study?
Does inactivation of the Car3 gene affect growth, development, life span, or response to oxidative stress in mice?
Does inactivation of the Car3 gene affect growth, development, life span, or response to oxidative stress in mice?
Carbonic anhydrase III is dispensable for normal growth, development, life span, and oxidative stress response in mice under standard laboratory conditions.
Answers are grounded in this paper and cite their sources.
Car3 is dispensable for normal mouse viability and oxidative stress response; leaves open its role in other contexts or species.
Carbonic anhydrase III is a cytosolic protein which is particularly abundant in skeletal muscle, adipocytes, and liver. The specific activity of this isozyme is quite low, suggesting that its physiological function is not that of hydrating carbon dioxide. To understand the cellular roles of carbonic anhydrase III, we inactivated the Car3 gene. Mice lacking carbonic anhydrase III were viable and fertile and had normal life spans. Carbonic anhydrase III has also been implicated in the response to oxidative stress. We found that mice lacking the protein had the same response to a hyperoxic challenge as did their wild-type siblings. No anatomic alterations were noted in the mice lacking carbonic anhydrase III. They had normal amounts and distribution of fat, despite the fact that carbonic anhydrase III constitutes about 30% of the soluble protein in adipocytes. We conclude that carbonic anhydrase III is dispensable for mice living under standard laboratory husbandry conditions.
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Kim et al. (2004) studied this question.
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