<i>Tex19.1</i> inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes

Reichmann, Judith; Dobie, Karen; Lister, Lisa; Crichton, James H; Best, Diana; MacLennan, Marie; Read, David; Raymond, Eleanor S; Hung, Chao-Chun; Boyle, Shelagh; Shirahige, Katsuhiko; Cooke, Howard J.; Herbert, Mary; Adams, Ian R.

doi:10.1083/jcb.201702123

Cited by 7 publications

(8 citation statements)

References 72 publications

(177 reference statements)

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“…In Drosophila , a proper nutrient state during oogenesis is critical for the establishment of the unique quiescent state of oocytes (Sieber et al, 2016 ). In mammals, primordial oocytes are retained in a quiescent state that is prolonged with aging, and proteostatic regulation during the primordial stage is critical for the long‐term maintenance of chromosomal cohesin (Burkhardt et al, 2016 ; Reichmann et al, 2020 ). Mouse oocytes have a functional insulin signaling cascade (Acevedo et al, 2007 ), which may be involved in the transcriptional response to CR.…”

Section: Discussionmentioning

confidence: 99%

Single‐oocyte transcriptome analysis reveals aging‐associated effects influenced by life stage and calorie restriction

et al. 2021

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Chromosome segregation errors in oocytes lead to the production of aneuploid eggs, which are the leading cause of pregnancy loss and of several congenital diseases such as Down syndrome. The frequency of chromosome segregation errors in oocytes increases with maternal age, especially at a late stage of reproductive life. How aging at various life stages affects oocytes differently remains poorly understood. In this study, we describe aging‐associated changes in the transcriptome profile of mouse oocytes throughout reproductive life. Our single‐oocyte comprehensive RNA sequencing using RamDA‐seq revealed that oocytes undergo transcriptome changes at a late reproductive stage, whereas their surrounding cumulus cells exhibit transcriptome changes at an earlier stage. Calorie restriction, a paradigm that reportedly prevents aging‐associated egg aneuploidy, promotes a transcriptome shift in oocytes with the up‐regulation of genes involved in chromosome segregation. This shift is accompanied by the improved maintenance of chromosomal cohesin, the loss of which is a hallmark of oocyte aging and causes chromosome segregation errors. These findings have implications for understanding how oocytes undergo aging‐associated functional decline throughout their reproductive life in a context‐dependent manner.

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Section: Discussionmentioning

confidence: 99%

Single‐oocyte transcriptome analysis reveals aging‐associated effects influenced by life stage and calorie restriction

et al. 2021

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“…The observation that mobilization of LINE-1 ( Long interspersed nuclear element 1) retrotransposons is restricted by TEX19.1 in mouse embryonic stem cells [ 44 ] may explain the placental dysfunction and small size. Lastly, it was recently reported that TEX19.1 maintains acetylated SMC3 (Structural Maintenance of Chromosome 3) and sister chromatid cohesion in postnatal oocytes and prevents aneuploidy [ 45 ].…”

Section: Tex Gene Expression and Function In The Mousementioning

confidence: 99%

Human testis-expressed (TEX) genes: a review focused on spermatogenesis and male fertility

Bellil

Ghieh

Hermel

et al. 2021

Basic Clin. Androl.

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Spermatogenesis is a complex process regulated by a multitude of genes. The identification and characterization of male-germ-cell-specific genes is crucial to understanding the mechanisms through which the cells develop. The term “TEX gene” was coined by Wang et al. (Nat Genet. 2001; 27: 422–6) after they used cDNA suppression subtractive hybridization (SSH) to identify new transcripts that were present only in purified mouse spermatogonia. TEX (Testis expressed) orthologues have been found in other vertebrates (mammals, birds, and reptiles), invertebrates, and yeasts. To date, 69 TEX genes have been described in different species and different tissues. To evaluate the expression of each TEX/tex gene, we compiled data from 7 different RNA-Seq mRNA databases in humans, and 4 in the mouse according to the expression atlas database.Various studies have highlighted a role for many of these genes in spermatogenesis. Here, we review current knowledge on the TEX genes and their roles in spermatogenesis and fertilization in humans and, comparatively, in other species (notably the mouse). As expected, TEX genes appear to have a major role in reproduction in general and in spermatogenesis in humans but also in all mammals such as the mouse. Most of them are expressed specifically or predominantly in the testis. As most of the TEX genes are highly conserved in mammals, defects in the male (gene mutations in humans and gene-null mice) lead to infertility. In the future, cumulative data on the human TEX genes’ physiological functions and pathophysiological dysfunctions should become available and is likely to confirm the essential role of this family in the reproductive process. Thirteen TEX genes are now referenced in the OMIM database, and 3 have been linked to a specific phenotype. TEX11 (on Xq13.1) is currently the gene most frequently reported as being associated with azoospermia.

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“…[ 26 ] TEX19.1 in mouse oocytes contributes to preventing homologue chromosome segregation errors and premature sister chromatid separation during meiosis I. [ 27 ] In the absence of TEX19.1, mouse oocytes missegregate their chromosomes during meiosis I and transmit aneuploidies to the next generation. [ 27 ] These post‐translational modifications are conserved in mammals, which may partially explain the high frequency of chromosome segregation errors in mammalian eggs.…”

Section: Introductionmentioning

confidence: 99%

Meiotic defects in human oocytes: Potential causes and clinical implications

Luo

et al. 2022

BioEssays

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Meiotic defects cause abnormal chromosome segregation leading to aneuploidy in mammalian oocytes. Chromosome segregation is particularly error-prone in human oocytes, but the mechanisms behind such errors remain unclear. To explain the frequent chromosome segregation errors, recent investigations have identified multiple meiotic defects and explained how these defects occur in female meiosis. In particular, we review the causes of cohesin exhaustion, leaky spindle assembly checkpoint (SAC), inherently unstable meiotic spindle, fragmented kinetochores or centromeres, abnormal aurora kinases (AURK), and clinical genetic variants in human oocytes. We mainly focus on meiotic defects in human oocytes, but also refer to the potential defects of female meiosis in mouse models.

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Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes

Cited by 7 publications

References 72 publications

Single‐oocyte transcriptome analysis reveals aging‐associated effects influenced by life stage and calorie restriction

Single‐oocyte transcriptome analysis reveals aging‐associated effects influenced by life stage and calorie restriction

Human testis-expressed (TEX) genes: a review focused on spermatogenesis and male fertility

Meiotic defects in human oocytes: Potential causes and clinical implications

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