Bcl-w is an antiapoptotic protein of the BCl-2 family. Like
BCL2, expressed BCLW promotes cell survival under a variety of cytotoxic conditions.
NCBI Summary:
This gene encodes a member of the BCL-2 protein family. The proteins of this family form hetero- or homodimers and act as anti- and pro-apoptotic regulators. Expression of this gene in cells has been shown to contribute to reduced cell apoptosis under cytotoxic conditions. Studies of the related gene in mice indicated a role in the survival of NGF- and BDNF-dependent neurons. Mutation and knockout studies of the mouse gene demonstrated an essential role in adult spermatogenesis.
General function
Cell death/survival, Anti-apoptotic
Comment
Cellular localization
Cytoplasmic, Mitochondrial
Comment
Ovarian function
Follicle atresia
Comment
Expression regulated by
Comment
Ovarian localization
Comment
Follicle stages
Antral, Preovulatory
Comment
Liu HC, et al 2001 reported tha application of complementary DNA microarray (DNA chip) technology in the study of gene expression profiles during
folliculogenesis.
They used oligonucleotide microarray (DNA chip)-based hybridization
analysis to gain a comprehensive view of gene expression and regulation
involved in folliculogenesis.
Preantral follicles isolated from day 14 B6D2F-1 mice
were stimulated in vitro to form Graafian follicles. Total RNA extracted from
the mouse preantral and Graafian follicles were reverse transcribed, labeled
with digoxigenin-11-dUTP, and then hybridized with Clontech Atlas mouse cDNA
expression arrays for comparison. Of 588 known studied genes, 39 and 61 were detected in preantral follicles and in Graafian follicles, respectively, and 17 were highly
expressed consistently in both preantral and Graafian follicles. Performing
clustering analysis, 46 were upregulated as the follicles advanced to mature stages. The BCLW gene is up-regulated in the Graafian follicles.
Phenotypes
Mutations
1 mutations
Species: mouse
Mutation name: None
type: null mutation fertility: fertile Comment:Ross et al. (1998) screened lines of mutant mice created
using a retroviral gene-trap system for male infertility. Homozygous ROSA41 male mice exhibited sterility associated
with progressive testicular degeneration. Germ cell defects were first observed at 19 days postnatal. Spermatogenesis
was blocked during late spermiogenesis in young adults. Gradual depletion of all stages of germ cells resulted in a
Sertoli-cell-only phenotype by approximately 6 months of age. Subsequently, almost all Sertoli cells were lost from the
seminiferous tubules, and the Leydig cell population was reduced. Molecular analysis indicated that the gene mutated in
these mice is BCLW, a death-protecting member of the Bcl2 family. The mutant allele of Bclw in ROSA41 did not
produce a Bclw polypeptide. Expression of Bclw in the testis appeared to be restricted to elongating spermatids and
Sertoli cells.