The spindle checkpoint rescues the meiotic segregation of chromosomes whose crossovers are far from the centromere

2007 ◽  
Vol 39 (10) ◽  
pp. 1273-1277 ◽  
Author(s):  
Soni Lacefield ◽  
Andrew W Murray
Keyword(s):  
Spindle Checkpoint ◽  
Meiotic Segregation ◽  
Segregation Of Chromosomes

A study of meiotic segregation of chromosomes in spermatozoa of translocation carriers using fluorescentin situhybridisation

Andrologia ◽  
2010 ◽  
Vol 42 (1) ◽  
pp. 27-34 ◽  
Author(s):  
A. Perrin ◽  
F. Morel ◽  
N. Douet-Guilbert ◽  
M.-J. Le Bris ◽  
J. Amice ◽  
...  
Keyword(s):  
Meiotic Segregation ◽  
Segregation Of Chromosomes

scholarly journals Mad1’s ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans

2021 ◽  
Author(s):  
Alice Devigne ◽  
Needhi Bhalla
Keyword(s):  
Nuclear Envelope ◽  
Meiotic Prophase ◽  
Nuclear Periphery ◽  
Spindle Checkpoint ◽  
Primary Role ◽  
Cis Acting ◽  
C Elegans ◽  
Meiotic Synapsis ◽  
Segregation Of Chromosomes

Meiotic homolog synapsis is essential to ensure accurate segregation of chromosomes during meiosis.  In C. elegans , synapsis and a checkpoint that monitors synapsis relies on the spindle checkpoint components, Mad1 and Mad2, and Pairing Centers (PCs), cis-acting loci that interact with the nuclear envelope to mobilize chromosomes within the nucleus. Here, we show that mutations in some spindle checkpoint mutants affect PC movement early in meiotic prophase, consistent with a link between PC mobility and the regulation of synapsis. Further, we test what specific functions of Mad1 and Mad2 are required to regulate and monitor synapsis. We find that a mutation that abrogates Mad1’s localization to the nuclear periphery abolishes the synapsis checkpoint but has no effect on Mad2’s localization to the nuclear periphery or synapsis. By contrast, a mutation that prevents Mad1’s interaction with Mad2 abolishes the synapsis checkpoint, delays synapsis and fails to localize Mad2 to the nuclear periphery. These data indicate that Mad1’s primary role in regulating synapsis is through control of Mad2 and that Mad2 can bind other factors at the nuclear periphery. We also tested whether Mad2’s ability to adopt a specific conformation associated with its activity during spindle checkpoint function is required for its role in meiosis. A mutation that prevents Mad2 from adopting its active conformer fails to localize to the nuclear periphery, abolishes the synapsis checkpoint and exhibits substantial defects in meiotic synapsis. Thus, Mad2, and its regulation by Mad1, is a major regulator of meiotic synapsis in C. elegans .

scholarly journals A knockout screen for protein kinases required for the proper meiotic segregation of chromosomes in the fission yeast Schizosaccharomyces pombe

Cell Cycle ◽  
2013 ◽  
Vol 12 (4) ◽  
pp. 618-624 ◽  
Author(s):  
Ines Kovacikova ◽  
Silvia Polakova ◽  
Zsigmond Benko ◽  
Lubos Cipak ◽  
Lijuan Zhang ◽  
...  
Keyword(s):  
Schizosaccharomyces Pombe ◽  
Fission Yeast ◽  
Protein Kinases ◽  
Meiotic Segregation ◽  
Segregation Of Chromosomes

scholarly journals Mad1’s ability to interact with Mad2 is essential to regulate and monitor meiotic synapsis in C. elegans

PLoS Genetics ◽  
2021 ◽  
Vol 17 (11) ◽  
pp. e1009598
Author(s):  
Alice Devigne ◽  
Needhi Bhalla
Keyword(s):  
Nuclear Envelope ◽  
Nuclear Periphery ◽  
Spindle Checkpoint ◽  
Primary Role ◽  
Cis Acting ◽  
C Elegans ◽  
Important Regulator ◽  
Meiotic Synapsis ◽  
Segregation Of Chromosomes

Meiotic homolog synapsis is essential to ensure accurate segregation of chromosomes during meiosis. In C. elegans, proper regulation of synapsis and a checkpoint that monitors synapsis relies on the spindle checkpoint components, Mad1 and Mad2, and Pairing Centers (PCs), cis-acting loci that interact with the nuclear envelope to mobilize chromosomes within the nucleus. Here, we test what specific functions of Mad1 and Mad2 are required to regulate and monitor synapsis. We find that a mutation that prevents Mad1’s localization to the nuclear periphery abolishes the synapsis checkpoint but has no effect on Mad2’s localization to the nuclear periphery or synapsis. By contrast, a mutation that prevents Mad1’s interaction with Mad2 abolishes the synapsis checkpoint, delays synapsis and fails to localize Mad2 to the nuclear periphery. These data indicate that Mad1’s primary role in regulating synapsis is through control of Mad2 and that Mad2 can bind other factors at the nuclear periphery. We also tested whether Mad2’s ability to adopt a specific conformation associated with its activity during spindle checkpoint function is required for its role in meiosis. A mutation that prevents Mad2 from adopting its active conformer fails to localize to the nuclear periphery, abolishes the synapsis checkpoint and exhibits substantial defects in meiotic synapsis. Thus, Mad2, and its regulation by Mad1, is an important regulator of meiotic synapsis in C. elegans.

Sign in / Sign up

Export Citation Format

Share Document