January 1, 2015
Correspondence: David Haig dhaig@oeb.harvard.edu
Author Affiliations
Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford Street, Cambridge 02138, MA, USA
BMC Biology 2014, 12:772 doi:10.1186/s12915-014-0104-2
More about author:
http://www.oeb.harvard.edu/faculty/haig/Home.htm
Commentary
Organisms evolve to maximize their genes’ chances of leaving descendant copies. In pursuit of this goal, some species live fast and die young while others adopt a more sedate pace of life. Life-history theory attempts to understand ecological factors that shape strategic allocations between size versus number of offspring, reproductive effort versus body maintenance, early versus delayed reproduction, and making the best of current opportunities versus preparing for an uncertain future. A major strategic decision involves the relative proliferation of cells contributing to muscle mass (conferring superior earning capacity but increased maintenance costs) and fat mass (a load to be carried but insurance against hard times). Antagonistic effects of Grb10 and Dlk1 appear to modulate this trade-off between productive investment and precautionary savings [1]. Of particular interest, these genes are oppositely imprinted: Grb10 is expressed from the allele a mouse inherits from its mother, but not the allele it inherits from its father, whereas Dlk1 is expressed when inherited from fathers but not mothers.
The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1741-7007/12/772
Related Research Article:
Antagonistic roles in fetal development and adult physiology for the oppositely imprinted Grb10 and Dlk1 genes
image source: Bacteria from Lean Humans Can Slim Obese Mice
