scholarly journals Defects in lamin B1 expression or processing affect interphase chromosome position and gene expression

2007 ◽  
Vol 176 (5) ◽  
pp. 593-603 ◽  
Author(s):  
Ashraf Malhas ◽  
Chiu Fan Lee ◽  
Rebecca Sanders ◽  
Nigel J. Saunders ◽  
David J. Vaux
Keyword(s):  
Gene Expression ◽  
Nuclear Lamina ◽  
Chromosome Territory ◽  
Full Length ◽  
Interphase Chromosome ◽  
Control Of Gene Expression ◽  
Lamin B1 ◽  
Chromosome Position ◽  
Normal Expression ◽  
The Stability

Radial organization of nuclei with peripheral gene-poor chromosomes and central gene-rich chromosomes is common and could depend on the nuclear boundary as a scaffold or position marker. To test this, we studied the role of the ubiquitous nuclear envelope (NE) component lamin B1 in NE stability, chromosome territory position, and gene expression. The stability of the lamin B1 lamina is dependent on lamin endoproteolysis (by Rce1) but not carboxymethylation (by Icmt), whereas lamin C lamina stability is not affected by the loss of full-length lamin B1 or its processing. Comparison of wild-type murine fibroblasts with fibroblasts lacking full-length lamin B1, or defective in CAAX processing, identified genes that depend on a stable processed lamin B1 lamina for normal expression. We also demonstrate that the position of mouse chromosome 18 but not 19 is dependent on such a stable nuclear lamina. The results implicate processed lamin B1 in the control of gene expression as well as chromosome position.

scholarly journals Co-dependence between trypanosome nuclear lamina components in nuclear stability and control of gene expression

2016 ◽  
Vol 44 (22) ◽  
pp. 10554-10570 ◽  
Author(s):  
Luke Maishman ◽  
Samson O. Obado ◽  
Sam Alsford ◽  
Jean-Mathieu Bart ◽  
Wei-Ming Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nuclear Lamina ◽  
Control Of Gene Expression ◽  
Stability And Control ◽  
Nuclear Stability ◽  
And Control

scholarly journals Progesterone depletion results in Lamin B1 loss and induction of cell death in mouse trophoblast giant cells

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254674
Author(s):  
Hiromu Morimoto ◽  
Misuzu Ueno ◽  
Hideyuki Tanabe ◽  
Tomohiro Kono ◽  
Hidehiko Ogawa
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Nuclear Lamina ◽  
Giant Cells ◽  
Specific Gene ◽  
Ploidy Levels ◽  
Lamin B1 ◽  
Trophoblast Giant Cells

Trophoblast giant cells (TGCs), a mouse trophoblast subtype, have large amounts of cytoplasm and high ploidy levels via endocycles. The diverse functions and gene expression profiles of TGCs have been studied well, but their nuclear structures remain unknown. In this study, we focus on Lamin B1, a nuclear lamina, and clarify its expression dynamics, regulation and roles in TGC functions. TGCs that differentiated from trophoblast stem cells were used. From days 0 to 9 after differentiation, the number of TGCs gradually increased, but the amount of LMNB1 peaked at day 3 and then slightly decreased. An immunostaining experiment showed that LMNB1-depleted TGCs increased after day 6 of differentiation. These LMNB1-depleted TGCs diffused peripheral localization of the heterochromatin marker H3K9me2 in the nuclei. However, LMINB1-knock down was not affected TGCs specific gene expression. We found that the death of TGCs also increased after day 6 of differentiation. Moreover, Lamin B1 loss and the cell death in TGCs were protected by 10−6 M progesterone. Our results conclude that progesterone protects against Lamin B1 loss and prolongs the life and function of TGCs.

scholarly journals Rhythmic chromatin interactions with lamin B1 reflect stochasticity in variable lamina-associated domains during the circadian cycle

2019 ◽  
Author(s):  
Annaël Brunet ◽  
Frida Forsberg ◽  
Philippe Collas
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Nuclear Lamina ◽  
Circadian Cycle ◽  
Chromatin Dynamics ◽  
Nuclear Lamins ◽  
Lamin B1 ◽  
Chromatin Interactions ◽  
Periodic Gene ◽  
Periodic Gene Expression

AbstractMany mammalian genes exhibit circadian expression patterns concordant with periodic binding of transcription factors, chromatin modifications and chromosomal interactions. Here, we report periodic interactions of chromatin with nuclear lamins, suggesting rhythmic associations with the nuclear lamina. Entrainment of the circadian clock is accompanied in mouse liver by a gain of lamin B1-chromatin interactions, followed by oscillations in these interactions at hundreds of lamina-associated domains (LADs). A subset of these oscillations exhibit distinct 12, 18, 24 or 30-h periodicity in our dataset, and affect one or both LAD borders or entire stand-alone LADs. However, most LADs are conserved during the circadian cycle, and periodic LADs are seldom occurrences rather than dominant features of variable LADs. Periodic LADs display oscillation asynchrony between 5’ and 3’ LAD borders, and are uncoupled from periodic gene expression within or in vicinity of these LADs. Accordingly, periodic genes, including central clock-control genes, are often located megabases away from LADs, suggesting residence in a transcriptionally permissive environment throughout the circadian cycle. Autonomous oscillatory associations of the genome with nuclear lamins provide new evidence for rhythmic spatial chromatin configurations. Nevertheless, our data suggest that periodic LADs reflect stochasticity in lamin-chromatin interactions underlying chromatin dynamics in the liver during the circadian cycle. They also argue that periodic gene expression is by and large not regulated by rhythmic chromatin associations with the nuclear lamina.

Abstract 508: Nuclear Lamins At Enhancers: A New Hypothesis for Laminopathies

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Kohta Ikegami ◽  
Stefano Secchia ◽  
Omar Almakki ◽  
Alexis V Stutzman ◽  
Sachie Ikegami ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Binding Sites ◽  
Nuclear Periphery ◽  
Nuclear Lamina ◽  
Lamin A ◽  
New Paradigm ◽  
Control Of Gene Expression ◽  
Nuclear Lamins ◽  
Nuclear Interior

The segregation of heterochromatin domains (LADs) at the nuclear periphery by the nuclear lamina, composed by polymerized nuclear Lamin A/C, provides a longstanding paradigm for the control of gene expression and for the mechanisms underlying Lamin-A/C-associated disorders, including progeria and cardiomyopathy. Here, we provide evidence supporting a novel paradigm that Lamin A/C functions as a transcription factor in the nuclear interior. We discovered that Ser22-phosphorylated Lamin A/C (pS22-Lamin A/C), required for lamin depolymerization during mitosis, populated the nuclear interior throughout the cell cycle. pS22-Lamin A/C ChIP-deq demonstrated localization at a large subset of putative active enhancers, not LADs. pS22-Lamin A/C-binding sites were co-occupied by the transcriptional activator c-Jun. In progeria patient-derived fibroblasts, a subset of pS22-Lamin A/C-binding sites were lost whereas new pS22-Lamin A/C-binding sites emerged. New pS22-Lamin A/C binding was accompanied by increased histone acetylation and increased c-Jun binding, whereas loss of pS22-Lamin A/C-binding was accompanied by loss of histone acetylation and c-Jun binding. New pS22-Lamin A/C enhancer binding in progeria was associated with upregulated expression of genes implicated in progeria pathophysiology, including cardiovascular disease. In contrast, alteration of LADs in progeria-patient cells could not explain the observed gene expression changes. These results suggest that Lamin A/C regulates gene expression by enhancer binding in the nuclear interior, independent of its function at the nuclear lamina, providing a new paradigm for the pathogenesis of lamin-associated disorders. pS22-Lamin A/C was also present in the nuclear interior of adult mouse cardiomyocytes. Cardiomyocyte-specific deletion of Lmna encoding Lamin A/C in adult mice caused extensive transcriptional changes in the heart and dilated cardiomyopathy, without apparent reduction of nuclear peripheral Lamin A/C. Disruption of the gene regulatory rather than LAD tethering function of Lamin A/C may underlie the pathogenesis of disorders caused by LMNA mutations, including cardiomyopathy.

Role of histone acetylation in the control of gene expression

2005 ◽  
Vol 83 (3) ◽  
pp. 344-353 ◽  
Author(s):  
Loredana Verdone ◽  
Micaela Caserta ◽  
Ernesto Di Mauro
Keyword(s):  
Gene Expression ◽  
Histone Acetylation ◽  
Dna Sequences ◽  
Control Of Gene Expression ◽  
Functional Roles ◽  
Lysine Residues ◽  
Human Disorders ◽  
Covalent Modifications ◽  
The Stability ◽  
Nuclear Processes

Histone proteins play structural and functional roles in all nuclear processes. They undergo different types of covalent modifications, defined in their ensemble as epigenetic because changes in DNA sequences are not involved. Histone acetylation emerges as a central switch that allows interconversion between permissive and repressive chromatin domains in terms of transcriptional competence. The mechanisms underlying the histone acetylation-dependent control of gene expression include a direct effect on the stability of nucleosomal arrays and the creation of docking sites for the binding of regulatory proteins. Histone acetyltransferases and deacetylases are, respectively, the enzymes devoted to the addition and removal of acetyl groups from lysine residues on the histone N-terminal tails. The enzymes exert fundamental roles in developmental processes and their deregulation has been linked to the progression of diverse human disorders, including cancer.Key words: gene expression, transcription, HATs, HDACs, nucleosome.

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