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HEAT-SHOCK TRANSCRIPTION FACTOR 2; HSF2 OKDB#: 1513
 Symbols: HEAT-SHOCK TRANSCRIPTION FACTOR 2; HSF2 Species: human
 Synonyms: HEAT-SHOCK FACTOR 2|  Locus: 6q22.3 in Homo sapiens


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General Comment When any organism is stressed by an increase in temperature, a set of protective proteins are synthesized that presumably function to maintain intracellular homeostasis. Transcription of heat-shock genes (e.g., OMIM 140550) is rapidly induced after temperature stress. This response is mediated by a promoter element, the heat-shock element (HSE). HSE binds a multimeric transcriptional stimulatory protein, termed heat-shock factor (HSF). Heat shock transcription factors activate heat-shock response genes under conditions of heat or other stresses. Using the partial peptide sequence of HSF1 from HeLa cells to screen a human T-cell cDNA library . HSF1 and HSF2 encode proteins that bind specifically to the heat-shock element and have homology to HSFs of other species.

NCBI Summary: HSF2, as well as the related gene HSF1, encodes a protein that binds specifically to the heat-shock element and has homology to HSFs of other species. Heat shock transcription factors activate heat-shock response genes under conditions of heat or other stresses. Although the names HSF1 and HSF2 were chosen for historical reasons, these peptides should be referred to as heat-shock transcription factors.
General function Nucleic acid binding, DNA binding, Transcription factor
Comment
Cellular localization Nuclear
Comment
Ovarian function Oogenesis
Comment
Expression regulated by
Comment
Ovarian localization Oocyte
Comment
Follicle stages
Comment
Phenotypes
Mutations 1 mutations

Species: mouse
Mutation name: None
type: null mutation
fertility: subfertile
Comment: Kallio M, et al 2002 reported brain abnormalities, defective meiotic chromosome synapsis and female subfertility in HSF2 null mice. Heat shock factor 2, one of the four vertebrate HSFs, transcriptional regulators of heat shock gene expression, is active during embryogenesis and spermatogenesis, with unknown functions and targets. By disrupting the Hsf2 gene, the authors show that, although the lack of HSF2 is not embryonic lethal, Hsf2(-/-) mice suffer from brain abnormalities, and meiotic and gametogenesis defects in both genders. The disturbances in brain are characterized by the enlargement of lateral and third ventricles and the reduction of hippocampus and striatum, in correlation with HSF2 expression in proliferative cells of the neuroepithelium and in some ependymal cells in adults. Hsf2(-/-) females suffer from multiple fertility defects: the production of abnormal eggs, the reduction in ovarian follicle number and the presence of hemorrhagic cystic follicles are consistent with meiotic defects. Hsf2(-/-) females also display hormone response defects, that can be rescued by superovulation treatment, and exhibit abnormal rates of luteinizing hormone receptor mRNAs. Hsf2-/- females were found to have dramatic ovulation problems. Only three Hsf2-/- females produced eggs, resulting in a total average of 3.5 eggs per Hsf2-/- female. Seven out of 10 Hsf2+/+ females ovulated with a total average of 7.4 eggs per female. The average number of fertilized eggs was 0.6 fertilized egg per Hsf2-/- female versus 4.9 per Hsf2+/+ female (P < 0.05). Indeed, Hsf2-/- females frequently produced abnormal eggs: 43.7% of the eggs were fragmented or without polar bodies (versus 5.4% for control females) or were unfertilized (40.6% with only one polar body versus 28.4% in controls). The authors attempted to rescue ovulation in Hsf2-/- females by administration of pregnant mare serum gonadotropin (PMSG/FSH)/human chorionic gonadotropin (hCG/LH) to 21- to 27-day-old mice, a treatment used to induce superovulation. All Hsf2-/- females were able to ovulate after this treatment. A total of 35.1 ? 22.5 eggs were ovulated by Hsf2-/- females (n = 16), statistically comparable (P = 0.853) with 37.2 ? 11.7 eggs in wild-type females (n = 5). However, while the eggs of wild-type females were able to develop in vitro to the two-cell stage with good scores (27.3 ? 1.7 eggs; 78.3% of the total ovulated eggs), eggs of Hsf2-/- females were often abnormal and only 10.2 ? 5.8 eggs (29.2% of the total) developed to the two-cell stage, which was significantly lower (P = 0.0132). The fact that 70% of the eggs ovulated by Hsf2-/- females were abnormal is suggestive of meiotic problems. Since superovulation treatment rescued ovulation in Hsf2-/- females, part of the ovarian defects observed in pubescent Hsf2-/- females may be secondary to disturbed hormonal physiological concentrations of gonadotropins or ovarian function alterations.

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created: June 4, 2002, 1:03 p.m. by: hsueh   email:
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last update: Sept. 20, 2006, 4:35 p.m. by: amazinmazin    email:



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