Sexual dimorphism in the width of the mouse synaptonemal complex

Agostinho, Ana; Kouznetsova, Anna; Hernández‐Hernández, Abrahan; Bernhem, Kristoffer; Blom, Hans; Brismar, Hjalmar; Höög, Christer

doi:10.1242/jcs.212548

Cited by 11 publications

(10 citation statements)

References 37 publications

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“…This distance may be optimal for the maintenance and resolution of meiotic recombination intermediates, and so an answer may lie in differences in recombination in the few meiotic organisms that lack an SC 1 . Interestingly, the SC central region and central element are approximately 10% narrower in female mice than in males 36 . This variation can be accommodated by the SYCP1 lattice that we propose through alteration in angulation of αN-end assemblies and αC-dimers (Supplementary Fig.…”

Section: Discussionmentioning

confidence: 95%

Structural basis of meiotic chromosome synapsis through SYCP1 self-assembly

Dunce

Dunne

Ratcliff

et al. 2018

Nat Struct Mol Biol

157

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Meiotic chromosomes adopt unique structures in which linear arrays of chromatin loops are bound together in homologous chromosome pairs by a supramolecular protein assembly, the synaptonemal complex. This three-dimensional scaffold provides the essential structural framework for genetic exchange by crossing over and subsequent homolog segregation. The core architecture of the synaptonemal complex is provided by SYCP1. Here we report the structure and self-assembly mechanism of human SYCP1 through X-ray crystallographic and biophysical studies. SYCP1 has an obligate tetrameric structure in which an N-terminal four-helical bundle bifurcates into two elongated C-terminal dimeric coiled-coils. This building block assembles into a zipper-like lattice through two self-assembly sites. N-terminal sites undergo cooperative head-to-head assembly in the midline, while C-terminal sites interact back to back on the chromosome axis. Our work reveals the underlying molecular structure of the synaptonemal complex in which SYCP1 self-assembly generates a supramolecular lattice that mediates meiotic chromosome synapsis.

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Section: Discussionmentioning

confidence: 95%

Structural basis of meiotic chromosome synapsis through SYCP1 self-assembly

Dunce

Dunne

Ratcliff

et al. 2018

Nat Struct Mol Biol

157

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“…One consequence of these differences might be a higher rate of ectopic synapsis and unequal crossover between these LCRs in female germ cells than in their male counterparts resulting in the observed maternal parent-of-origin bias for type-1 NF1 deletions. An intriguing sexual dimorphism has recently been observed pertaining to the width of the synaptonemal complex in the mouse (Agostinho et al 2018). The synaptonemal complex is a proteinaceous tripartite, ladder-like structure that links homologous chromosomes and mediates recombination, in particular crossover formation, during meiotic prophase I (reviewed by Zickler and Kleckner, 2015).…”

Section: Discussionmentioning

confidence: 99%

Pronounced maternal parent-of-origin bias for type-1 NF1 microdeletions

et al. 2018

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Neurofibromatosis type 1 (NF1) is caused, in 4.7-11% of cases, by large deletions encompassing the NF1 gene and its flanking regions within 17q11.2. Different types of large NF1 deletion occur which are distinguishable by their breakpoint location and underlying mutational mechanism. Most common are the type-1 NF1 deletions of 1.4 Mb which exhibit recurrent breakpoints caused by nonallelic homologous recombination (NAHR), also termed unequal crossover. Here, we analyzed 37 unrelated families of patients with de novo type-1 NF1 deletions by means of short tandem repeat (STR) profiling to determine the parental origin of the deletions. We observed that 33 of the 37 type-1 deletions were of maternal origin (89.2% of cases; p < 0.0001). Analysis of the patients' siblings indicated that, in 14 informative cases, ten (71.4%) deletions resulted from interchromosomal unequal crossover during meiosis I. Our findings indicate a strong maternal parent-of-origin bias for type-1 NF1 deletions. A similarly pronounced maternal transmission bias has been reported for recurrent copy number variants (CNVs) within 16p11.2 associated with autism, but not so far for any other NAHR-mediated pathogenic CNVs. Region-specific genomic features are likely to be responsible for the maternal bias in the origin of both the 16p11.2 CNVs and type-1 NF1 deletions.

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“…However, some of the axial and lateral element mutants display no defects in fertility suggesting that the structure and possibly the composition of the SC may be different in each sex. Since no sex-specific SC proteins have been identified yet, the composition of the SC appears to be the same between male and female mice (Agostinho et al 2018). Despite this similar protein composition, the width or distance between the lateral elements of the SC is ~ 60 nm shorter in females than in males (Agostinho et al 2018).…”

Section: Leptotene: Formation Of the Meiotic Chromosome Axes And Doubmentioning

confidence: 99%

“…Since no sex-specific SC proteins have been identified yet, the composition of the SC appears to be the same between male and female mice (Agostinho et al 2018). Despite this similar protein composition, the width or distance between the lateral elements of the SC is ~ 60 nm shorter in females than in males (Agostinho et al 2018). This decrease in SC width in female mice is likely the result of positioning the transverse filament protein, SYCP1, deeper into the lateral element, thereby suggesting that the organization of the proteins within the lateral element may differ in females (Agostinho et al 2018).…”

Section: Leptotene: Formation Of the Meiotic Chromosome Axes And Doubmentioning

confidence: 99%

“…Despite this similar protein composition, the width or distance between the lateral elements of the SC is ~ 60 nm shorter in females than in males (Agostinho et al 2018). This decrease in SC width in female mice is likely the result of positioning the transverse filament protein, SYCP1, deeper into the lateral element, thereby suggesting that the organization of the proteins within the lateral element may differ in females (Agostinho et al 2018). Moreover, sex-specific differences in SC width is not unique to mice.…”

Section: Leptotene: Formation Of the Meiotic Chromosome Axes And Doubmentioning

confidence: 99%

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Leagues of their own: sexually dimorphic features of meiotic prophase I

Cahoon

Libuda

2019

Chromosoma

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Meiosis is a conserved cell division process that is used by sexually reproducing organisms to generate haploid gametes. Males and females produce different end products of meiosis: eggs (females) and sperm (males). In addition, these unique end products demonstrate sex-specific differences that occur throughout meiosis to produce the final genetic material that is packaged into distinct gametes with unique extracellular morphologies and nuclear sizes. These sexually dimorphic features of meiosis include the meiotic chromosome architecture, in which both the lengths of the chromosomes and the requirement for specific meiotic axis proteins being different between the sexes. Moreover, these changes likely cause sex-specific changes in the recombination landscape with the sex that has the longer chromosomes usually obtaining more crossovers. Additionally, epigenetic regulation of meiosis may contribute to sexually dimorphic recombination landscapes. Here we explore the sexually dimorphic features of both the chromosome axis and crossing over for each stage of meiotic prophase I in Mus musculus, Caenorhabditis elegans, and Arabidopsis thaliana. Furthermore, we consider how sex-specific changes in the meiotic chromosome axes and the epigenetic landscape may function together to regulate crossing over in each sex, indicating that the mechanisms controlling crossing over may be different in oogenesis and spermatogenesis.

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Sexual dimorphism in the width of the mouse synaptonemal complex

Cited by 11 publications

References 37 publications

Structural basis of meiotic chromosome synapsis through SYCP1 self-assembly

Structural basis of meiotic chromosome synapsis through SYCP1 self-assembly

Pronounced maternal parent-of-origin bias for type-1 NF1 microdeletions

Leagues of their own: sexually dimorphic features of meiotic prophase I

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