prmt-5

Caenorhabditis elegans

Enables DNA-binding transcription factor binding activity; p53 binding activity; and protein methyltransferase activity. Involved in several processes, including intrinsic apoptotic signaling pathway in response to DNA damage; negative regulation of DNA damage response, signal transduction by p53 class mediator; and response to odorant. Located in nucleus. Part of transcription repressor complex. Human ortholog(s) of this gene implicated in Leydig cell tumor and seminoma. Is an ortholog of human PRMT5 (protein arginine methyltransferase 5).

Mettl13

Mus musculus

PHENOTYPE: Mice heterozygous for a null allele exhibit infertility, bilateral cryptorchism, abnormal spermatogenesis, and increased Leydig cell number. [provided by MGI curators]

Bcl2l2

Mus musculus

PHENOTYPE: Homozygous null mutants are male sterile with progressive loss of germ cells, Sertoli cells and Leydig cells beginning at puberty. [provided by MGI curators]

Ddx25

Mus musculus

PHENOTYPE: Homozygous null mice display male infertility, arrest of spermatogenesis at step 8, abnormal Leydig cells, and increased germ cell apoptosis in males. [provided by MGI curators]

H3f4

Mus musculus

PHENOTYPE: Mice homozygous for a knock-out allele exhibit male infertility associated with small testes, meiotic failure, increased male germ cell apoptosis, and azoospermia. Male homozygotes for a different knock-out allele show impaired spermatogenesis, an expanded testicular interstitium, seminiferous tubule atrophy, increased Leydig and Sertoli cell numbers, and enhanced testosterone synthesis along with cellular senescence in Leydig cells. [provided by MGI curators]

Cdkn2c

Mus musculus

PHENOTYPE: Homozygotes for targeted null mutations exhibit kidney and mammary gland cortical cysts, Leydig cell hyperplasia, reduced testosterone levels, late developing thymic lymphomas and pituitary tumors, gigantism, and organomegaly. [provided by MGI curators]

Lhcgr

Homo sapiens

This gene encodes the receptor for both luteinizing hormone and choriogonadotropin. This receptor belongs to the G-protein coupled receptor 1 family, and its activity is mediated by G proteins which activate adenylate cyclase. Mutations in this gene result in disorders of male secondary sexual character development, including familial male precocious puberty, also known as testotoxicosis, hypogonadotropic hypogonadism, Leydig cell adenoma with precocious puberty, and male pseudohermaphtoditism with Leydig cell hypoplasia. [provided by RefSeq, Jul 2008]

Acsbg1

Mus musculus

PHENOTYPE: Mice homozygous for a null mutation display abnormalities in gonadotropin induced changes in testosterone production, Leydig cell morphology and long chain and very long chain fatty acid levels. [provided by MGI curators]

E2f6

Mus musculus

PHENOTYPE: Both homozygous and heterozygous null mice exhibit subtle posterior transformations of the axial skeleton with incomplete penetrance. In addition to skeletal transformations, male mice homozygous for one knock-out allele display defective spermatocyte development and Leydig cell hyperplasia. [provided by MGI curators]

Dmrt1

Mus musculus

PHENOTYPE: Males homozygous for null mutations are sterile and exhibit a complete loss of germ cells between postnatal days 7-14, disorganized seminiferous tubules, and degeneration of Leydig cells. Females are normal and fertile. [provided by MGI curators]