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

• DOI: 10.1128/mcb.20.20.7773-7783.2000
• Publication Date: 2002-07-27T10:06:23Z
• Authors: Harry Scherthan; Martin Jerratsch; Sonu Dhar; Y. Alan Wang; Stephen P. Goff; Tej K. Pandita
• Keywords: Cell Nucleus; Male; Mice, Knockout; 0301 basic medicine; Nuclear Proteins; Cell Cycle Proteins; Ataxia Telangiectasia Mutated Proteins; Genes, p53; Immunohistochemistry; Chromatin; DNA-Binding Proteins; Histones; Ataxia Telangiectasia; Meiosis; Mice; 03 medical and health sciences; Heterochromatin; Animals; Nuclear Matrix; Gene Deletion; In Situ Hybridization, Fluorescence; Fluorescent Dyes

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 as well Atm(-/-) mice are predisposed cancer infertile due spermatogenesis disruption during first meiotic prophase. spermatocytes frequently display aberrant synapsis clustered telomeres (bouquet topology). Here, we used telomere fluorescent in situ hybridization immunofluorescence (IF) staining SCP3 testes-specific histone H1 (H1t) Atm- Atm-p53-deficient investigated whether gonadal atrophy Atm-null associated stalling motility SCP3-H1t IF revealed most p53(-/-) degenerated late zygotene, while a few progressed pachytene diplotene some even beyond metaphase II, indicated by presence round spermatids. In meiosis, frequency I bouquet topology was elevated 72-fold. Bouquet were generally void H1t signals, mid-late displayed expression showed dispersed over nuclear periphery. Thus, it appears movements occur independently ATM signaling. Atm inactivation more likely leads accumulation slowing progression through initial stages prophase ensuing arrest demise I. Sertoli cells (SECs), which contribute faithful spermatogenesis, mutants found numerous heterochromatin clusters-a resembles immature SECs. However, SECs exhibited mature vimentin cytokeratin 8 intermediate filament signature. Upon antibodies, observed signals throughout nuclei human mouse SECs, I, haploid but not absent from elongating spermatid nuclei. be removed prior occurrence DNA nicks emanate consequence nucleoprotamine formation.