SGOL2

Shugoshin-like 2 (S. pombe), also known as SGOL2, is a protein which in humans is encoded by the SGOL2 gene.[5][6]

SGO2
Identifiers
AliasesSGO2, TRIPIN, SGOL2, shugoshin 2
External IDsOMIM: 612425 MGI: 1098767 HomoloGene: 51867 GeneCards: SGO2
Gene location (Human)
Chr.Chromosome 2 (human)[1]
Band2q33.1Start200,510,008 bp[1]
End200,584,096 bp[1]
Orthologs
SpeciesHumanMouse
Entrez

151246

68549

Ensembl

ENSG00000163535

ENSMUSG00000026039

UniProt

Q562F6

Q7TSY8

RefSeq (mRNA)

NM_001160033
NM_001160046
NM_152524

NM_001177867
NM_199007

RefSeq (protein)

NP_001153505
NP_001153518
NP_689737

NP_001171338
NP_950172

Location (UCSC)Chr 2: 200.51 – 200.58 MbChr 1: 58 – 58.03 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

Shugoshin-like 2 (SGOL2) is one of the two mammalian orthologs of the Shugoshin/Mei-S322 family of proteins that regulate sister chromatid cohesion by protecting the integrity of a multiprotein complex named cohesin.[7] This protective system is essential for faithful chromosome segregation during mitosis and meiosis, which is the physical basis of Mendelian inheritance.

Model organisms

Model organisms have been used in the study of SGOL2 function. A conditional knockout mouse line, called Sgol2tm1a(EUCOMM)Wtsi[12][13] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists — at the Wellcome Trust Sanger Institute.[14][15][16] Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[10][17] Twenty two tests were carried out on mutant mice but no significant abnormalities were observed.[10]

Using another genetically engineered mouse that lacks Sgol2 function, and siRNA experiments in oocytes, it has been shown that disruption of the mouse SGOL2 does not cause any alteration in sister chromatid cohesion in embryonic cultured fibroblasts and adult somatic tissues. Moreover, although these mutant mice also develop normally and survive to adulthood without any apparent alteration, both male and female Sgol2-deficient mice from this line are infertile.[18] By different approaches it was demonstrated that SGOL2 is necessary for protecting centromeric cohesion during mammalian meiosis I.[18] In vivo, the loss of SGOL2 promotes a premature release of the meiosis-specific REC8 cohesin complexes from anaphase I centromeres.[19] This molecular alteration is manifested cytologically by the complete loss of centromere cohesion at metaphase II leading to single chromatids and physiologically with the formation of aneuploid gametes that give rise to infertility.

References
  1. GRCh38: Ensembl release 89: ENSG00000163535 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000026039 - Ensembl, May 2017
  3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. "Entrez Gene: SGOL2 shugoshin-like 2 (S. pombe)".
  6. Kitajima TS; Kawashima SA; Watanabe Y (February 2004). "The conserved kinetochore protein shugoshin protects centromeric cohesion during meiosis". Nature. 427 (6974): 510–7. doi:10.1038/nature02312. PMID 14730319. S2CID 4400426.
  7. Kitajima TS; Sakuno T; Ishiguro K; Iemura S; Natsume T; Kawashima SA; Watanabe Y (May 2006). "Shugoshin collaborates with protein phosphatase 2A to protect cohesin". Nature. 441 (7089): 46–52. doi:10.1038/nature04663. PMID 16541025. S2CID 4425074.
  8. "Salmonella infection data for Sgol2". Wellcome Trust Sanger Institute.
  9. "Citrobacter infection data for Sgol2". Wellcome Trust Sanger Institute.
  10. Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88 (S248). doi:10.1111/j.1755-3768.2010.4142.x. S2CID 85911512.
  11. Mouse Resources Portal, Wellcome Trust Sanger Institute.
  12. "International Knockout Mouse Consortium".
  13. "Mouse Genome Informatics".
  14. Skarnes, W. C.; Rosen, B.; West, A. P.; Koutsourakis, M.; Bushell, W.; Iyer, V.; Mujica, A. O.; Thomas, M.; Harrow, J.; Cox, T.; Jackson, D.; Severin, J.; Biggs, P.; Fu, J.; Nefedov, M.; De Jong, P. J.; Stewart, A. F.; Bradley, A. (2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–342. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  15. Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  16. Collins FS; Rossant J; Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. S2CID 18872015.
  17. van der Weyden L; White JK; Adams DJ; Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biol. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.
  18. Llano E; Gómez R; Gutiérrez-Caballero C; Herrán Y; Sánchez-Martín M; Vázquez-Quiñones L; Hernández T; de Alava E; Cuadrado A; Barbero JL; Suja JA; Pendás AM (September 2008). "Shugoshin-2 is essential for the completion of meiosis but not for mitotic cell division in mice". Genes Dev. 22 (17): 2400–13. doi:10.1101/gad.475308. PMC 2532928. PMID 18765791.
  19. Lee J; Kitajima TS; Tanno Y; Yoshida K; Morita T; Miyano T; Miyake M; Watanabe Y (January 2008). "Unified mode of centromeric protection by shugoshin in mammalian oocytes and somatic cells". Nat. Cell Biol. 10 (1): 42–52. doi:10.1038/ncb1667. PMID 18084284. S2CID 39482208.

Further reading
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.