Recently appointed faculty member, Susan Maloney, just published findings on the Nf1 gene and its role in mouse social behavior. Loss of Nf1 in humans causes neurofibromatosis, a disease which results in non-malign tumors of the CNS and other tissues. More recently, it has been recognized that about half of NF patients also have autism.

Susan and co. investigated how loss of Nf1 in mice regulated youth social behavior and monoamine levels. Whole-organism loss of Nf1 led to increased serotonin and decreased vocalizations, independent of neurofibromatosis pathologic markers, suggesting that Nf1 “moonlights” in an additional role in structural organization or regulation of social behaviors in the brain. Interestingly, knocking Nf1 only out of astrocytes–brain support cells–resulted in the opposite, suggesting that Nf1 has distinct and cell-type specific activities in controlling such behaviors. Great work, Susan!