Genetic control of social organization in an ant

A central issue in evolutionary biology is the extent to which complex social organization is under genetic control. We have found that a single genomic element marked by the protein-encoding gene Gp-9 is responsible for the existence of two distinct forms of social organization in the fire ant Solenopsis invicta. This genetic factor influences the reproductive phenotypes and behavioral strategies of queens and determines whether workers tolerate a single fertile queen or multiple queens per colony. Furthermore, this factor affects worker tolerance of queens with alternate genotypes, thus explaining the dramatic differences in Gp-9 allele frequencies observed between the two social forms in the wild. These findings reveal how a single genetic factor can have major effects on complex social behavior and influence the nature of social organization.

Oxytocin is required for nursing but is not essential for parturition or reproductive behavior.

Oxytocin, a neurohypophyseal hormone, has been traditionally considered essential for mammalian reproduction. In addition to uterine contractions during labor and milk ejection during nursing, oxytocin has been implicated in anterior pituitary function, paracrine effects in the testis and ovary and the neural control of maternal and sexual behaviors. To determine the essential role(s) of oxytocin in mammalian reproductive function, mice deficient in oxytocin have been generated using embryonic stem cell technology. A deletion of exon 1 encoding the oxytocin peptide was generated in embryonic stem cells at a high frequency and was successfully transmitted in the germ line. Southern blot analysis of genomic DNA from homozygote offspring and in situ hybridization with an exonic probe 3' of the deletion failed to detect any oxytocin or neurophysin sequences, respectively, confirming that the mutation was a null mutation. Mice lacking oxytocin are both viable and fertile. Males do not have any reproductive behavioral or functional defects in the absence of oxytocin. Similarly, females lacking oxytocin have no obvious deficits in fertility or reproduction, including gestation and parturition. However, although oxytocin-deficient females demonstrate normal maternal behavior, all offspring die shortly after birth because of the dam's inability to nurse. Postpartum injections of oxytocin to the oxytocin deficient mothers restore milk ejection and rescue the offspring. Thus, despite the multiple reproductive activities that have been attributed to oxytocin, oxytocin plays an essential role only in milk ejection in the mouse.