Differences in DNA double strand breaks repair in male germ cell types: Lessons learned from a differential expression of Mdc1 and 53BP1

Ahmed, Emad A.; Vaart, Aniek van der; Barten, Angeliqué; Kal, Henk B.; Chen, Junjie; Lou, Zhenkun; Minter-Dykhouse, Katherine; Bártková, Jiřina; Bártek, Jiří; Boer, P. de

doi:10.1016/j.dnarep.2007.02.011

Cited by 89 publications

(72 citation statements)

References 41 publications

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“…These results are in agreement with the known decrease in radiosensitivity of maturing male germ cells, which has been linked to chromatin condensation and replacement of histones with protamines in these cells [Joshi et al, 1990;van Loon et al, 1993;Haines et al, 1998]. In addition, they reflect the proficiency of testicular cells in both Non Homologous End Joining (NHEJ) and Homologous Recombination (HR)-mediated repair [Srivastava and Raman, 2007;Ahmed et al, 2007Ahmed et al, , 2010a. Despite the initial repair of DNA damage in testicular cells, a subsequent time-course analysis of DNA damage between 7 and 45 days after irradiation revealed the appearance of delayed DNA lesions in both testicular cells and sperm.…”

Section: Discussionsupporting

confidence: 85%

“…Phosphorylated H2AX (g-H2AX) foci are markers of DNA double strand breaks [Rogakou et al, 1998]. g-H2AX content in testicular cells is heterogeneous, higher than in cells from other organs and increases after irradiation [Hamer et al, 2003;Ahmed et al, 2007Ahmed et al, , 2010aBlanco-Rodriguez, 2009;Paris et al, 2011]. The presence of H2AX has been documented in human [Gatewood et al, 1990] and in mouse [Meyer-Ficca et al, 2009] sperm chromatin.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, it is interesting to speculate whether there is a common denominator between differentiating spermatogonia and early meiotic cells that may be affecting their susceptibility to radiation-induced delayed effects. Proliferating spermatogonia have several features that define them as a unique testicular subpopulation: replicative DNA synthesis, mitotic activity, chromatin organization, DNA repair pathways, and radiosensitivity [van der Meer et al, 1992;Ahmed et al, 2007;Rube et al, 2011]. DNA synthesis also occurs in preleptotene spermatocytes, and in zygotene/ pachytene spermatocytes where it is associated with the repair of double strand breaks introduced during the homology search process [Kidane et al, 2010].…”

Section: Discussionmentioning

confidence: 99%

“…The sensitivity of male germ cells to ionizing radiation depends on the differentiation stage, chromatin condensation, nucleoproteins composition, and variation in repair capacity at the time of exposure [Spanò et al, 1987;Beumer et al, 1997;Ahmed et al, 2007Ahmed et al, , 2010a. Direct ionization of cellular macromolecules, particularly DNA, or indirect damage to these macromolecules via reactive oxygen species produced by water radiolysis, can cause cell death, DNA damage, chromosome aberrations, and mutations.…”

Section: Introductionmentioning

confidence: 99%

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Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

Cordelli¹,

Eleuteri²,

Grollino³

et al. 2012

Environ and Mol Mutagen

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Sperm DNA integrity is essential for the accurate transmission of paternal genetic information. Various stages of spermatogenesis are characterized by large differences in radiosensitivity. Differentiating spermatogonia are susceptible to radiationinduced cell killing, but some of them can repair DNA damage and progress through differentiation. In this study, we applied the neutral comet assay, immunodetection of phosphorylated H2AX (g-H2AX) and the Sperm Chromatin Structure Assay (SCSA) to detect DNA strand breaks in testicular cells and spermatozoa at different times following in vivo X-ray irradiation. Radiation produced DNA strand breaks in testicular cells that were repaired within the first few hours after exposure. Spermatozoa were resistant to the induction of DNA damage, but non-targeted DNA lesions were detected in spermatozoa derived from surviving irradiated spermatogonia. These lesions formed while round spermatids started to elongate within the testicular seminiferous tubules. The transcription of pro-apoptotic genes at this time was also enhanced, suggesting that an apoptotic-like process was involved in DNA break production. Our results suggest that proliferating spermatogonia retain a memory of the radiation insult that is recognized at a later developmental stage and activates a process leading to DNA fragmentation. Environ. Mol. Mutagen. 53:429-439, 2012. V V C 2012 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

Cordelli¹,

Eleuteri²,

Grollino³

et al. 2012

Environ and Mol Mutagen

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show abstract

“…These include BRCA1, BRCA2, BLM, MDC1, TOPBP1, 53BP1 and RAD1. [102][103][104][105][106][107][108] The above-mentioned post replication repair enzyme HR6B and its E3 ligase partner RAD18 also accumulate on the XY body. 109 All of these proteins, except BLM, 53BP1 and the RAD18/ HR6A/B complex, also accumulate on the meiotic DSBs shortly after their formation in leptotene.…”

mentioning

confidence: 99%

DNA double strand break repair, chromosome synapsis and transcriptional silencing in meiosis

Inagaki

Schoenmakers²,

Baarends³

2010

Epigenetics

105

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C hromosome pairing and synapsis during meiotic prophase requires the formation and repair of DNA double-strand breaks (DSBs) by the topoisomerase-like enzyme SPO11. Chromosomes, or chromosomal regions, that lack a pairing partner, such as the largely heterologous X and Y chromosomes, show delayed meiotic DSB repair and are transcriptionally silenced. Herein, we review meiosis-specific aspects of DSB repair in relation to homology recognition and meiotic silencing of heterologous regions. We propose a dynamic interplay between progression of synapsis and persistent meiotic DSBs. Signaling from these persistent breaks could inhibit heterologous synapsis and stimulate meiotic silencing of the X and Y chromosomes.

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The management of DNA double‐strand breaks in mitotic G₂, and in mammalian meiosis viewed from a mitotic G₂ perspective

Burgoyne¹,

Mahadevaiah²,

Turner³

2007

BioEssays

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DNA double-strand breaks (DSBs) are extremely hazardous lesions for all DNA-bearing organisms and the mechanisms of DSB repair are highly conserved. In the eukaryotic mitotic cell cycle, DSBs are often present following DNA replication while, in meiosis, hundreds of DSBs are generated as a prelude to the reshuffling of the maternally and paternally derived genomes. In both cases, the DSBs are repaired by a process called homologous recombinational repair (HRR), which utilises an intact DNA molecule as the repair template. Mitotic and meiotic HRR are managed by 'checkpoints' that inhibit cell division until DSB repair is complete. Here we attempt to summarise the substantial recent progress in understanding the checkpoint management of HRR in mitosis (focussing mainly on mammals) and then go on to use this information as a framework for understanding the presumed checkpoint management of HRR in mammalian meiosis.

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Differences in DNA double strand breaks repair in male germ cell types: Lessons learned from a differential expression of Mdc1 and 53BP1

Cited by 89 publications

References 41 publications

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

DNA double strand break repair, chromosome synapsis and transcriptional silencing in meiosis

The management of DNA double‐strand breaks in mitotic G₂, and in mammalian meiosis viewed from a mitotic G₂ perspective

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Differences in DNA double strand breaks repair in male germ cell types: Lessons learned from a differential expression of Mdc1 and 53BP1

Cited by 89 publications

References 41 publications

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

Direct and delayed X‐ray‐induced DNA damage in male mouse germ cells

DNA double strand break repair, chromosome synapsis and transcriptional silencing in meiosis

The management of DNA double‐strand breaks in mitotic G2, and in mammalian meiosis viewed from a mitotic G2 perspective

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The management of DNA double‐strand breaks in mitotic G₂, and in mammalian meiosis viewed from a mitotic G₂ perspective