HA95 and LAP2β mediate a novel chromatin–nuclear envelope interaction implicated in initiation of DNA replication

Martins, Sandra; Eikvar, Sissel; Furukawa, Kazuhiro; Collas, Philippe

doi:10.1083/jcb.200210026

Cited by 66 publications

(66 citation statements)

References 38 publications

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“…However, in the analysis between arsenical skin lesion cases (n = 11) and noncases (n = 5), we found 3.3-fold up-regulation of thymopoietin, a gene that has been implicated in the initiation of DNA replication (55). Furthermore, an in vitro study found that thymopoietin was overexpressed in cancer cell lines (56).…”

Section: Discussionmentioning

confidence: 93%

Gene Expression Profiles in Peripheral Lymphocytes by Arsenic Exposure and Skin Lesion Status in a Bangladeshi Population

Argos¹,

Kibriya²,

Parvez

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Millions of individuals worldwide are chronically exposed to arsenic through their drinking water. In this study, the effect of arsenic exposure and arsenical skin lesion status on genome-wide gene expression patterns was evaluated using RNA from peripheral blood lymphocytes of individuals selected from the Health Effects of Arsenic Longitudinal Study. Affymetrix HG-U133A GeneChip (Affymetrix, Santa Clara, CA) arrays were used to measure the expression of f22,000 transcripts. Our primary statistical analysis involved identifying differentially expressed genes between participants with and without arsenical skin lesions based on the significance analysis of microarrays statistic with an a priori defined 1% false discovery rate to minimize false positives. To better characterize differential expression, we also conducted Gene Ontology and pathway comparisons in addition to the gene-specific analyses. Fourhundred sixty-eight genes were differentially expressed between these two groups, from which 312 differentially expressed genes were identified by restricting the analysis to female never-smokers. We also explored possible differential gene expression by arsenic exposure levels among individuals without manifest arsenical skin lesions; however, no differentially expressed genes could be identified from this comparison. Our findings show that microarray-based gene expression analysis is a powerful method to characterize the molecular profile of arsenic exposure and arsenic-induced diseases. Genes identified from this analysis may provide insights into the underlying processes of arsenic-induced disease and represent potential targets for chemoprevention studies to reduce arsenicinduced skin cancer in this population.

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Section: Discussionmentioning

confidence: 93%

Gene Expression Profiles in Peripheral Lymphocytes by Arsenic Exposure and Skin Lesion Status in a Bangladeshi Population

Argos¹,

Kibriya²,

Parvez

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…LBR targeting to chromosomes may be the trigger for attaching membranes to chromatin and may initiate nuclear membrane assembly. Other membrane proteins, such as emerin and LAP2β may then diffuse within the lipid bilayer and form stable complexes at the chromatin surface by specific interactions with BAF, HA95 (Martins et al, 2003), heterochromatin protein 1 (HP1, Ye and Worman, 1996), histones (Goldberg et al, 1999;Polioudaki et al, 2001;Taniura et al, 1995) or DNA (for a review, see Vlcek et al, 2001). …”

Section: Discussionmentioning

confidence: 99%

LAP2α and BAF transiently localize to telomeres and specific regions on chromatin during nuclear assembly

Dechat

Gajewski

Korbei

et al. 2004

Journal of Cell Science

Self Cite

185

203

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Lamina-associated polypeptide (LAP) 2α is a LEM (lamina-associated polypeptide emerin MAN1) family protein associated with nucleoplasmic A-type lamins and chromatin. Using live cell imaging and fluorescence microscopy we demonstrate that LAP2α was mostly cytoplasmic in metaphase and associated with telomeres in anaphase. Telomeric LAP2α clusters grew in size, formed `core' structures on chromatin adjacent to the spindle in telophase, and translocated to the nucleoplasm in G1 phase. A subfraction of lamin C and emerin followed LAP2α to the core region early on, whereas LAP2β, lamin B receptor and lamin B initially bound to more peripheral regions of chromatin, before they spread to core structures with different kinetics. Furthermore, the DNA-crosslinking protein barrier-to-autointegration factor (BAF) bound to LAP2α in vitro and in mitotic extracts, and subfractions of BAF relocalized to core structures with LAP2α. We propose that LAP2α and a subfraction of BAF form defined complexes in chromatin core regions and may be involved in chromatin reorganization during early stages of nuclear assembly.

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“…Furthermore, disruption of normal lamin organization by microinjection of a dominant-negative lamin A mutant results in inhibition of both DNA replication (Spann et al, 1997) and RNA polymerase II-dependent transcription (Spann et al, 2002) suggesting a role for lamin A in both these processes. Finally, lamins have the ability to bind directly to DNA (Stierle et al, 2003) and to chromatin (Glass et al, 1993;Taniura et al, 1995) and indirectly via associations with proteins containing a LEM box (Lee et al, 2001;Martins et al, 2003). Thus, the list of possible functions of the A-type lamins includes maintenance of nuclear structural integrity, organisation of higher-order chromatin structure and control of gene expression (Hutchison, 2002).…”

Section: Introductionmentioning

confidence: 99%

Aging of Hutchinson–Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis

Bridger

Kill

2004

Experimental Gerontology

155

136

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Hutchinson -Gilford progeria syndrome is a rare genetic disorder that mimics certain aspects of aging prematurely. Recent work has revealed that mutations in the lamin A gene are a cause of the disease. We show here that cellular aging of Hutchinson -Gilford progeria syndrome fibroblasts is characterised by a period of hyperproliferation and terminates with a large increase in the rate of apoptosis. The occurrence of cells with abnormal nuclear morphology reported by others is shown to be a result of cell division since the fraction of these abnormalities increases with cellular age. Similarly, the proportion of cells with an abnormal or absent A-type lamina increases with age. These data provide clues as to the cellular basis for premature aging in HGPS and support the view that cellular senescence and tissue homeostasis are important factors in the normal aging process. q 2004 Elsevier Inc. All rights reserved.

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HA95 and LAP2β mediate a novel chromatin–nuclear envelope interaction implicated in initiation of DNA replication

Cited by 66 publications

References 38 publications

Gene Expression Profiles in Peripheral Lymphocytes by Arsenic Exposure and Skin Lesion Status in a Bangladeshi Population

Gene Expression Profiles in Peripheral Lymphocytes by Arsenic Exposure and Skin Lesion Status in a Bangladeshi Population

LAP2α and BAF transiently localize to telomeres and specific regions on chromatin during nuclear assembly

Aging of Hutchinson–Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis

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