scholarly journals HIM-8 Binds to the X Chromosome Pairing Center and Mediates Chromosome-Specific Meiotic Synapsis

Cell ◽  
2005 ◽  
Vol 123 (6) ◽  
pp. 1051-1063 ◽  
Author(s):  
Carolyn M. Phillips ◽  
Chihunt Wong ◽  
Needhi Bhalla ◽  
Peter M. Carlton ◽  
Pinky Weiser ◽  
...  
Keyword(s):  
X Chromosome ◽  
Chromosome Pairing ◽  
Meiotic Synapsis ◽  
Pairing Center

Synaptic mutants in hexaploid oats (Avena sativa L.)

Genome ◽  
1988 ◽  
Vol 30 (1) ◽  
pp. 1-7 ◽  
Author(s):  
H. W. Rines ◽  
S. S. Johnson
Keyword(s):  
Chromosome Pairing ◽  
Sodium Azide ◽  
Avena Sativa ◽  
Seed Set ◽  
Single Gene ◽  
Inheritance Pattern ◽  
Late Prophase ◽  
Homologous Chromosomes ◽  
Breeding Station ◽  
Meiotic Synapsis

Three meiotic synapsis-deficient mutants of oats (Avena sativa L.) were analyzed to determine their inheritance pattern, detailed chromosomal behavior, and location to chromosome. These highly sterile mutants, one in the cultivar 'Stout' and two in 'Noble', had been recovered from progeny of sodium azide mutagenized populations. Each segregated as a single gene recessive. The only synapsis-deficient variants previously described in hexaploid oats have been nullisomics or ditelosomics. Mutant 'Stout 1212' was classified as asynaptic due to deficiencies in chromosome pairing at all meiotic stages. Mutants 'Noble 1362' and 'Noble 1911' were classified as desynaptic since their homologous chromosomes were paired in early meiosis but they disassociated prematurely in late prophase I. Using a partial monosomic series from the Welsh Plant Breeding Station, mutant 1212 was mapped to monosome XII and is probably a mutation in Syn-5, a gene previously defined only by its nulli effect. Mutants 1362 and 1911 were mapped to monosome IV and are probably mutations in Syn-1, a gene also previously defined only by its nulli effect. Seed set on the synaptic mutant plants in the field was less than 0.2% of that on fertile sibs and likely resulted from pollination by surrounding fertile plants. This seed may serve as a source of unique aneuploid stocks in oats.Key words: meiotic mutants, gene mapping, monosomics, nullisomics, oat cytogenetics.

scholarly journals A cis-acting locus that promotes crossing over between X chromosomes in Caenorhabditis elegans.

Genetics ◽  
1994 ◽  
Vol 136 (3) ◽  
pp. 887-902 ◽  
Author(s):  
A M Villeneuve
Keyword(s):  
Caenorhabditis Elegans ◽  
X Chromosome ◽  
Sharp Decrease ◽  
Crossing Over ◽  
Meiotic Pairing ◽  
X Chromosomes ◽  
Cis Acting ◽  
Pairing Site ◽  
High Level ◽  
Pairing Center

Abstract This study reports the characterization of a cis-acting locus on the Caenorhabditis elegans X chromosome that is crucial for promoting normal levels of crossing over specifically between the X homologs and for ensuring their proper disjunction at meiosis I. The function of this locus is disrupted by the mutation me8, which maps to the extreme left end of the X chromosome within the region previously implicated by studies of X; A translocations and X duplications to contain a meiotic pairing site. Hermaphrodites homozygous for a deletion of the locus (Df/Df) or heterozygous for a deletion and the me8 mutation (me8/Df) exhibit extremely high level of X chromosome nondisjunction at the reductional division; this is correlated with a sharp decrease in crossing over between the X homologs as evidenced both by reductions in genetic map distances and by the presence of achiasmate chromosomes in cytological preparations of oocyte nuclei. Duplications of the wild-type region that are unlinked to the X chromosome cannot complement the recombination and disjunction defects in trans, indicating that this region must be present in cis to the X chromosome to ensure normal levels of crossing over and proper homolog disjunction. me8 homozygotes exhibit an altered distribution of crossovers along the X chromosome that suggests a defect in processivity along the X chromosome of an event that initiates at the chromosome end. Models are discussed in which the cis-acting locus deleted by the Dfs functions as a meiotic pairing center that recruits trans-acting factors onto the chromosomes to nucleate assembly of a crossover-competent complex between the X homologs. This pairing center might function in the process of homolog recognition, or in the initiation of homologous synapsis.

scholarly journals Lack of detectable genetic recombination on the X chromosome during the parthenogenetic production of female and male aphids

2002 ◽  
Vol 79 (3) ◽  
pp. 203-209 ◽  
Author(s):  
DINAH F. HALES ◽  
ALEX C. C. WILSON ◽  
MATHEW A. SLOANE ◽  
JEAN-CHRISTOPHE SIMON ◽  
JEAN-FRANÇOIS LEGALLIC ◽  
...  
Keyword(s):  
X Chromosome ◽  
Chromosome Pairing ◽  
Reproductive Strategies ◽  
Genetic Recombination ◽  
Full Range ◽  
Nucleolar Organizer ◽  
Male Production ◽  
Cyclical Parthenogenesis ◽  
X Chromosomes ◽  
Polymorphic Microsatellite

We used polymorphic microsatellite markers to look for recombination during parthenogenetic oogenesis between the X chromosomes of aphids of the tribe Macrosiphini. We examined the X chromosome because it comprises ∼25% of the genome and previous cytological observations of chromosome pairing and nucleolar organizer (NOR) heteromorphism suggest recombination, although the same is not true for autosomes. A total of 564 parthenogenetic females of Myzus clones with three distinct reproductive modes (cyclical parthenogenesis, obligate parthenogenesis and obligate parthenogenesis with male production) were genotyped at three informative X-linked loci. Also, parthenogenetically produced males from clones encompassing the full range of male-producing reproductive strategies were genotyped. These included 391 Myzus persicae males that were genotyped at three X-linked loci and 538 males from Sitobion clones that were genotyped at five informative X-linked loci. Our results show no departure from clonality in parthenogenetic generations of aphids of the tribe Macrosiphini: no recombinant genotypes were observed in parthenogenetically produced males or females.

Chromosomal fusion and meiotic behaviour in Delena cancerides (Araneae: Sparassidae). I. Chromosome pairing and X-chromosome segregation

Genome ◽  
1991 ◽  
Vol 34 (4) ◽  
pp. 561-566 ◽  
Author(s):  
D. M. Rowell
Keyword(s):  
Synaptonemal Complex ◽  
Chromosome Segregation ◽  
X Chromosome ◽  
Chromosome Pairing ◽  
X Chromosomes ◽  
Translocation Heterozygote ◽  
Complex Translocation ◽  
Monobrachial Homology ◽  
Pairing Initiation ◽  
Surface Spreading

Surface spreading of meiotic material in Delena cancerides indicates that pairing initiation among metacentric chromosomes with monobrachial homology differs from that of telocentric forms and free metacentric bivalents and results in a star-shaped structure at pachytene. Distance cosegregation of the three X chromosomes in ancestral, telocentric forms is prefaced by a centric association early in prophase I. This centric association of the X chromosomes is conserved in metacentric races despite the presence of an X-autosome fusion.Key words: synaptonemal complex, translocation heterozygote, X chromosome, spider.

scholarly journals DNA damage response protein TOPBP1 regulates X chromosome silencing in the mammalian germ line

2017 ◽  
Vol 114 (47) ◽  
pp. 12536-12541 ◽  
Author(s):  
Elias ElInati ◽  
Helen R. Russell ◽  
Obah A. Ojarikre ◽  
Mahesh Sangrithi ◽  
Takayuki Hirota ◽  
...  
Keyword(s):  
Dna Damage ◽  
X Chromosome ◽  
Sex Chromosome ◽  
Germ Line ◽  
Direct Interaction ◽  
Critical Factor ◽  
Dna Double Strand Breaks ◽  
Meiotic Silencing ◽  
Meiotic Sex Chromosome Inactivation ◽  
Meiotic Synapsis

Meiotic synapsis and recombination between homologs permits the formation of cross-overs that are essential for generating chromosomally balanced sperm and eggs. In mammals, surveillance mechanisms eliminate meiotic cells with defective synapsis, thereby minimizing transmission of aneuploidy. One such surveillance mechanism is meiotic silencing, the inactivation of genes located on asynapsed chromosomes, via ATR-dependent serine-139 phosphorylation of histone H2AFX (γH2AFX). Stimulation of ATR activity requires direct interaction with an ATR activation domain (AAD)-containing partner. However, which partner facilitates the meiotic silencing properties of ATR is unknown. Focusing on the best-characterized example of meiotic silencing, meiotic sex chromosome inactivation, we reveal this AAD-containing partner to be the DNA damage and checkpoint protein TOPBP1. Conditional TOPBP1 deletion during pachynema causes germ cell elimination associated with defective X chromosome gene silencing and sex chromosome condensation. TOPBP1 is essential for localization to the X chromosome of silencing “sensors,” including BRCA1, and effectors, including ATR, γH2AFX, and canonical repressive histone marks. We present evidence that persistent DNA double-strand breaks act as silencing initiation sites. Our study identifies TOPBP1 as a critical factor in meiotic sex chromosome silencing.

Evidence that homologous X-chromosome pairing requires transcription and Ctcf protein

2007 ◽  
Vol 39 (11) ◽  
pp. 1390-1396 ◽  
Author(s):  
Na Xu ◽  
Mary E Donohoe ◽  
Susana S Silva ◽  
Jeannie T Lee
Keyword(s):  
X Chromosome ◽  
Chromosome Pairing

The initiation of meiotic chromosome pairing: the cytological view

Genome ◽  
1990 ◽  
Vol 33 (6) ◽  
pp. 759-778 ◽  
Author(s):  
Josef Loidl
Keyword(s):  
Synaptonemal Complex ◽  
Chromosome Pairing ◽  
Meiotic Chromosome ◽  
Meiotic Pairing ◽  
Cytological Evidence ◽  
Homologous Chromosomes ◽  
Synaptonemal Complex Formation ◽  
Meiotic Synapsis ◽  
The One ◽  
First Contact

Opposing views are held with respect to the time when and the mechanisms whereby homologous chromosomes find each other for meiotic synapsis. On the one hand, some evidence has been presented for somatic homologous associations or some other kind of relationship between chromosomes in somatic cells as a preliminary to meiotic pairing. On the other hand, it is argued by many that homologous contacts are first established at meiotic prophase prior to, or in the course of, synaptonemal complex formation. The present paper reviews the controversial cytological evidence, hypotheses, and ideas on how the first contact between homologous chromosomes comes about.Key words: synapsis, meiosis, presynaptic alignment, homologous recognition, synaptonemal complex, chromosome pairing.

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