Interphase Chromosome Arrangement in Sertoli Cells of Adult Mice1

Guttenbach, Martina; Martínez-Expósito, M.J.; Engel, Wolfgang; Schmid, Michael

doi:10.1095/biolreprod54.5.980

Cited by 19 publications

(17 citation statements)

References 39 publications

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“…2I). In Sertoli cells, KIN17 staining was concentrated in the two perinucleolar satellites in which the centromeric region of the chromosomes and the telomeric sequences of the short arms are clustered (Guttenbach et al, 1996) (Fig. 2H,K).…”

Section: Expression Of Mouse Kin17 Gene During Testicular Developmentmentioning

confidence: 99%

KIN17 encodes an RNA-binding protein and is expressed during mouse spermatogenesis

Pinon‐Lataillade

Masson

Bernardino-Sgherri

et al. 2004

Journal of Cell Science

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Genotoxic agents deform DNA structure thus eliciting a complex genetic response allowing recovery and cell survival. The Kin17 gene is up-regulated during this response. This gene encodes a conserved nuclear protein that shares a DNA-binding domain with the bacterial RecA protein. The KIN17 protein binds DNA and displays enhanced expression levels in proliferating cultured cells, suggesting a role in nuclear metabolism. We investigated this by studying the expression profile of KIN17 protein during mouse spermatogenesis. As expected, the expression level of Kin17 is higher in proliferating than in differentiated cells. KIN17 is selectively extracted from this tissue by detergents and a fraction was tightly associated with the nuclear matrix. Germinal cells ubiquitously express Kin17 and the protein is located mainly in the nucleus except in elongated spermatids where cytoplasmic staining is also observed. Sertoli and germ cells that are no longer mitotically active express KIN17, suggesting a general role in all testicular cell types. In adult testis a significant proportion of KIN17 co-purifies with polyadenylated RNA. KIN17 directly binds RNA, preferentially poly(G) and poly(U) homopolymers. These results together with the identification of KIN17 as a component of the human spliceosome indicate that this protein may participate in RNA processing.

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Section: Expression Of Mouse Kin17 Gene During Testicular Developmentmentioning

confidence: 99%

KIN17 encodes an RNA-binding protein and is expressed during mouse spermatogenesis

Pinon‐Lataillade

Masson

Bernardino-Sgherri

et al. 2004

Journal of Cell Science

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“…Using vimentin IF as an SEC marker on DAPI-stained testis preparations, we found that 79% or more of Atm Ϫ/Ϫ and Atm Ϫ/Ϫ p53 Ϫ/Ϫ SEC nuclei contained four or more heterochromatin clusters of various sizes (Fig. 6d), which represents a threefold increase over the control (Table 3) and data in the literature (37,41). It appears that the chromocenter distribution in Atm-mutant SECs is reminiscent of that of immature SECs (16).…”

Section: Control C-ablmentioning

confidence: 50%

“…It appears that the chromocenter distribution in Atm-mutant SECs is reminiscent of that of immature SECs (16). In addition to SECs with multiple heterochromatin clusters, both mutants contained a reduced number of SECs with two heterochromatin clusters, which are the predominant SEC type in the adult mouse (Table 3) (37,38).…”

Section: Control C-ablmentioning

confidence: 96%

“…In adult testes, most SECs display a unique nuclear architecture in that they carry a large nucleolus which is associated with one to three prominent DAPIbright heterochromatin clusters amidst a faintly stained euchromatin (Fig. 6a to c) (37,38,41). In contrast to the adult situation, most SEC nuclei of prepubertal mouse testes contain numerous heterochromatin clusters (16).…”

Section: Control C-ablmentioning

confidence: 98%

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Meiotic Telomere Distribution and Sertoli Cell Nuclear Architecture Are Altered in Atm- andAtm-p53-Deficient Mice

Scherthan

Jerratsch

Dhar

et al. 2000

Molecular and Cellular Biology

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The ataxia telangiectasia mutant (ATM) protein is an intrinsic part of the cell cycle machinery that surveys genomic integrity and responses to genotoxic insult. Individuals with ataxia telangiectasia as well as Atm ؊/؊ mice are predisposed to cancer and are infertile due to spermatogenesis disruption during first meiotic prophase. Atm ؊/؊ spermatocytes frequently display aberrant synapsis and clustered telomeres (bouquet topology). Here, we used telomere fluorescent in situ hybridization and immunofluorescence (IF) staining of SCP3 and testes-specific histone H1 (H1t) to spermatocytes of Atm-and Atm-p53-deficient mice and investigated whether gonadal atrophy in Atm-null mice is associated with stalling of telomere motility in meiotic prophase. SCP3-H1t IF revealed that most Atm ؊/؊ p53 ؊/؊ spermatocytes degenerated during late zygotene, while a few progressed to pachytene and diplotene and some even beyond metaphase II, as indicated by the presence of a few round spermatids. In Atm ؊/؊ p53 ؊/؊ meiosis, the frequency of spermatocytes I with bouquet topology was elevated 72-fold. Bouquet spermatocytes with clustered telomeres were generally void of H1t signals, while mid-late pachytene and diplotene Atm ؊/؊ p53 ؊/؊ spermatocytes displayed expression of H1t and showed telomeres dispersed over the nuclear periphery. Thus, it appears that meiotic telomere movements occur independently of ATM signaling. Atm inactivation more likely leads to accumulation of spermatocytes I with bouquet topology by slowing progression through initial stages of first meiotic prophase and an ensuing arrest and demise of spermatocytes I. Sertoli cells (SECs), which contribute to faithful spermatogenesis, in the Atm mutants were found to frequently display numerous heterochromatin and telomere clusters-a nuclear topology which resembles that of immature SECs. However, Atm ؊/؊ SECs exhibited a mature vimentin and cytokeratin 8 intermediate filament expression signature. Upon IF with ATM antibodies, we observed ATM signals throughout the nuclei of human and mouse SECs, spermatocytes I, and haploid round spermatids. ATM but not H1t was absent from elongating spermatid nuclei. Thus, ATM appears to be removed from spermatid nuclei prior to the occurrence of DNA nicks which emanate as a consequence of nucleoprotamine formation.Ataxia telangiectasia is a rare human recessive autosomal disorder with a pleiotropic phenotype, specifically including progressive neurological degeneration, telangiectasia, often associated with premature aging, reduced size, immunodeficiency, sensitivity to ionizing radiation, cancer predisposition, and infertility (13,40,81,93). Mice mutated in the homologue of the ATM (ataxia telangiectasia mutated) gene (Atm) display similar pleiotropic defects (5, 27, 97). The ATM protein belongs to a growing family of phosphatidylinositol-3 kinaserelated kinases and seems to play a role as an intrinsic part of the cell cycle machinery that surveys genomic integrity, cell cycle progression, and processing of DNA damage. It shows sim...

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“…First, centromeres are often positioned at the periphery of nucleoli in cultured cells (Guttenbach et al, 1996;Padeken et al, 2013) and the association has been functionally linked to chromatin silencing and genome stability (Padeken et al, 2013). Second, the key centromere assembly factor CAL1 and its functional human homologue Holliday junction recognition protein (HJURP), as well as human CENP-C (CENPC), localise to both centromeres and nucleoli (Dunleavy et al, 2009;Erhardt et al, 2008;Foltz et al, 2009;Pluta and Earnshaw, 1996;Wong et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Nucleolar activity and CENP-C regulate CENP-A and CAL1 availability for centromere assembly in meiosis

Kwenda¹,

Collins²,

Dattoli³

et al. 2016

Journal of Cell Science

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The centromere-specific histone CENP-A is the key epigenetic determinant of centromere identity. Whereas most histones are removed from mature sperm, CENP-A is retained to mark paternal centromeres. In Drosophila males we show that the centromere assembly factors CAL1 and CENP-C are required for meiotic chromosome segregation, CENP-A assembly and maintenance on sperm, as well as fertility. In meiosis, CENP-A accumulates with CAL1 in nucleoli. Furthermore, we show that CENP-C normally limits the release of CAL1 and CENP-A from nucleoli for proper centromere assembly in meiotic prophase I. Finally, we show that RNA polymerase I transcription is required for efficient CENP-A assembly in meiosis, as well as centromere tethering to nucleoli.

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Interphase Chromosome Arrangement in Sertoli Cells of Adult Mice1

Cited by 19 publications

References 39 publications

KIN17 encodes an RNA-binding protein and is expressed during mouse spermatogenesis

KIN17 encodes an RNA-binding protein and is expressed during mouse spermatogenesis

Meiotic Telomere Distribution and Sertoli Cell Nuclear Architecture Are Altered in Atm- andAtm-p53-Deficient Mice

Nucleolar activity and CENP-C regulate CENP-A and CAL1 availability for centromere assembly in meiosis

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