Species: mouse
Mutation name: None
type: null mutation
fertility: subfertile
Comment: Suppression of tumor angiogenesis by Galpha13 haploinsufficiency. Chen L et al. Heterotrimeric G proteins are critical transducers of cellular signaling. Among the four families of G proteins, the physiological function of Galpha13 is less well understood. Galpha13 gene-deleted mice died at embryonic stage ~9.5. Here we show that heterozygous Galpha13+/- mice displayed defects in adult angiogenesis. Female Galpha13+/- mice show a higher number of immature follicles and a lower density of blood vessels in mature corpus luteum comparing with Galpha13+/+ mice. Furthermore, implanted tumors grew slower in Galpha13+/- host mice. These tumor tissues had much less blood vessels comparing those from Galpha13+/+ host mice. Moreover, bone marrow-derived progenitor cells from Galpha13+/+ mice, when reconstituted into irradiated Galpha13+/- mice, rescued the failed growth of allografted tumors in Galpha13+/- mice. Hence, Galpha13 is haploinsufficient for adult angiogenesis, both in the female reproductive system and in tumor angiogenesis.