Asset Details
Do you wish to reserve the book?
Cdc20 Is Critical for Meiosis I and Fertility of Female Mice
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Cdc20 Is Critical for Meiosis I and Fertility of Female Mice
Do you wish to request the book?
Cdc20 Is Critical for Meiosis I and Fertility of Female Mice
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Cdc20 Is Critical for Meiosis I and Fertility of Female Mice
2010
Overview
Chromosome missegregation in germ cells is an important cause of unexplained infertility, miscarriages, and congenital birth defects in humans. However, the molecular defects that lead to production of aneuploid gametes are largely unknown. Cdc20, the activating subunit of the anaphase-promoting complex/cyclosome (APC/C), initiates sister-chromatid separation by ordering the destruction of two key anaphase inhibitors, cyclin B1 and securin, at the transition from metaphase to anaphase. The physiological significance and full repertoire of functions of mammalian Cdc20 are unclear at present, mainly because of the essential nature of this protein in cell cycle progression. To bypass this problem we generated hypomorphic mice that express low amounts of Cdc20. These mice are healthy and have a normal lifespan, but females produce either no or very few offspring, despite normal folliculogenesis and fertilization rates. When mated with wild-type males, hypomorphic females yield nearly normal numbers of fertilized eggs, but as these embryos develop, they become malformed and rarely reach the blastocyst stage. In exploring the underlying mechanism, we uncover that the vast majority of these embryos have abnormal chromosome numbers, primarily due to chromosome lagging and chromosome misalignment during meiosis I in the oocyte. Furthermore, cyclin B1, cyclin A2, and securin are inefficiently degraded in metaphase I; and anaphase I onset is markedly delayed. These results demonstrate that the physiologically effective threshold level of Cdc20 is high for female meiosis I and identify Cdc20 hypomorphism as a mechanism for chromosome missegregation and formation of aneuploid gametes.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Carrier Proteins - metabolism
/ Cell Biology/Cell Growth and Division
/ Cell Cycle Proteins - genetics
/ Cell Cycle Proteins - metabolism
/ Chromosomes, Mammalian - metabolism
/ Developmental Biology/Germ Cells
/ Female
/ Genetics and Genomics/Chromosome Biology
/ Genetics and Genomics/Genetics of Disease
/ Infertility, Female - genetics
/ Male
/ Meiosis
/ Mice
/ Protein Processing, Post-Translational
/ Proteins
/ Securin
We currently cannot retrieve any items related to this title. Kindly check back at a later time.