|malonyl CoA:ACP acyltransferase (mitochondrial)||OKDB#: 4310|
|Synonyms:||MT, MCT, fabD, NET62, FASN2C, MGC47838,||Locus:||22q13.31 in Homo sapiens|
For retrieval of Nucleotide and Amino Acid sequences please go to:
Mammalian Reproductive Genetics Endometrium Database Resource Orthologous Genes UCSC Genome Browser GEO Profilesnew!
R-L INTERACTIONS MGI
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link to BioGPS
NCBI Summary: The protein encoded by this gene is found exclusively in the mitochondrion, where it catalyzes the transfer of a malonyl group from malonyl-CoA to the mitochondrial acyl carrier protein. The encoded protein may be part of a fatty acid synthase complex that is more like the type II prokaryotic and plastid complexes rather than the type I human cytosolic complex. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq]
|Expression regulated by|
|Comment||MCAK regulates chromosome alignment but is not necessary for preventing aneuploidy in mouse oocyte meiosis I. Illingworth C et al. Errors in chromosome segregation in mammalian oocytes lead to aneuploid eggs that are developmentally compromised. In mitotic cells, mitotic centromere associated kinesin (MCAK; KIF2C) prevents chromosome segregation errors by detaching incorrect microtubule-kinetochore interactions. Here, we examine whether MCAK is involved in spindle function in mouse oocyte meiosis I, and whether MCAK is necessary to prevent chromosome segregation errors. We find that MCAK is recruited to centromeres, kinetochores and chromosome arms in mid-meiosis I, and that MCAK depletion, or inhibition using a dominant-negative construct, causes chromosome misalignment. However, the majority of oocytes complete meiosis I and the resulting eggs retain the correct number of chromosomes. Moreover, MCAK-depleted oocytes can recover from mono-orientation of homologous kinetochores in mid-meiosis I to segregate chromosomes correctly. Thus, MCAK contributes to chromosome alignment in meiosis I, but is not necessary for preventing chromosome segregation errors. Although other correction mechanisms may function in mammalian meiosis I, we speculate that late establishment of kinetochore microtubules in oocytes reduces the likelihood of incorrect microtubule-kinetochore interactions, bypassing the requirement for error correction.|
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Aaron J Hsueh,
home page: http://reprobio.stanford.edu/hsueh
|last update:||2010-06-02 08:02:44||by:||Aaron J Hsueh, hsuehlab email: firstname.lastname@example.org|