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Gene Review

Acvr2a  -  activin receptor IIA

Mus musculus

Synonyms: ACTR-IIA, ActRIIa, Activin receptor type IIA, Activin receptor type-2A, ActrIIa, ...
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Psychiatry related information on Acvr2a

  • Adult activin receptor type II null (Acvr2-/-) male mice display multiple reproductive behavioral deficits, including delayed initiation of copulation, reduced mount, and intromission frequencies, and increased mount, intromission, and ejaculation latencies [1].

High impact information on Acvr2a


Biological context of Acvr2a

  • In the absence of its subfamily receptor Acvr2a, however, the development of Acvr2b(4/4) mice was arrested at the gastrulation stage, recapitulating the Acvr2a(-/-); Acvr2b(+/-) mutant phenotype [5].
  • Fluorescent in situ localization of the bovine activin receptor type IIA locus on chromosome 2 (2q2.3-2.4) [6].

Anatomical context of Acvr2a

  • Activin receptor IIA is widely expressed in the male reproductive axis, including the pituitary and testis [4].
  • Activin receptor IIA-null male mice are fertile, have suppressed pituitary and serum FSH levels, and demonstrate a decrease in testis size as a result of reduced Sertoli cells and germ cells [4].
  • Activin has a positive growth effect on gonadal tumor cells in culture and directly causes the cancer cachexia-like syndrome in inhibin-deficient mice via interaction with activin receptor type IIA in livers and stomachs [7].
  • The impairment in behavior can be correlated to the nitric oxide content in the CNS because Acvr2-/- males have decreased NOS activity in the mPOA but not the rest of the hypothalamus or cortex [1].

Regulatory relationships of Acvr2a

  • In contrast to FSHbeta mRNA expression changes, pituitary FSH content was significantly reduced in Acvr2 null mice whereas it was only slightly upregulated in inhibin alpha null mice [8].

Other interactions of Acvr2a

  • Compared to castrated wild-type (WT) mice, FSHbeta mRNA levels in the pituitaries of Acvr2 null mice were significantly downregulated in the absence of gonadal feedback [8].
  • FSHbeta mRNA levels were not significantly higher in the pituitaries of castrated inhibin alpha null mice compared to those in Acvr2 null mice and remained the same in the pituitaries of castrated double mutant mice lacking both inhibin and ACVR2 [8].
  • Olfactory acuity tests confirmed that Acvr2-/- mice have no defects in general odor or pheromone recognition [1].


  1. Impaired male sexual behavior in activin receptor type II knockout mice. Ma, X., Reyna, A., Mani, S.K., Matzuk, M.M., Kumar, T.R. Biol. Reprod. (2005) [Pubmed]
  2. Expression of activin subunits, activin receptors and follistatin in postimplantation mouse embryos suggests specific developmental functions for different activins. Feijen, A., Goumans, M.J., van den Eijnden-van Raaij, A.J. Development (1994) [Pubmed]
  3. Bone morphogenetic protein (BMP) type II receptor deletion reveals BMP ligand-specific gain of signaling in pulmonary artery smooth muscle cells. Yu, P.B., Beppu, H., Kawai, N., Li, E., Bloch, K.D. J. Biol. Chem. (2005) [Pubmed]
  4. Male reproductive phenotypes in double mutant mice lacking both FSHbeta and activin receptor IIA. Kumar, T.R., Varani, S., Wreford, N.G., Telfer, N.M., de Kretser, D.M., Matzuk, M.M. Endocrinology (2001) [Pubmed]
  5. Generation of activin receptor type IIB isoform-specific hypomorphic alleles. Lee, Y.J., Hong, K.H., Yun, J., Oh, S.P. Genesis (2006) [Pubmed]
  6. Fluorescent in situ localization of the bovine activin receptor type IIA locus on chromosome 2 (2q2.3-2.4). Monteagudo, L.V., Heriz, A., Flavin, N., Rogers, M., Ennis, S., Arruga, M.V. Mamm. Genome (1996) [Pubmed]
  7. Follistatin is a modulator of gonadal tumor progression and the activin-induced wasting syndrome in inhibin-deficient mice. Cipriano, S.C., Chen, L., Kumar, T.R., Matzuk, M.M. Endocrinology (2000) [Pubmed]
  8. Regulation of FSHbeta and GnRH receptor gene expression in activin receptor II knockout male mice. Kumar, T.R., Agno, J., Janovick, J.A., Conn, P.M., Matzuk, M.M. Mol. Cell. Endocrinol. (2003) [Pubmed]
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