scholarly journals Microscopic notes on the perinucleolar chromatin region in immature and mature human B-leukemia lymphocytes

Neoplasma ◽  
2013 ◽  
Vol 60 (03) ◽  
pp. 284-289 ◽  
Author(s):  
K. SMETANA ◽  
J. KARBAN ◽  
I. JIRASKOVA ◽  
H. KLAMOVA ◽  
M. TRNENY
Keyword(s):  
Chromatin Region

News & Notes: Stochastic Nucleosome Positioning in a Yeast Chromatin Region Is Not Dependent on Histone H1

1999 ◽  
Vol 39 (3) ◽  
pp. 168-172 ◽  
Author(s):  
Sergi Puig ◽  
Emilia Matallana ◽  
José E. Pérez-Ortín
Keyword(s):  
Nucleosome Positioning ◽  
Histone H1 ◽  
Chromatin Region

scholarly journals Histone H3 Acetylation and H3 K4 Methylation Define Distinct Chromatin Regions Permissive for Transgene Expression

2006 ◽  
Vol 26 (17) ◽  
pp. 6357-6371 ◽  
Author(s):  
Chunhong Yan ◽  
Douglas D. Boyd
Keyword(s):  
Histone Modifications ◽  
Transgene Expression ◽  
De Novo ◽  
Histone H3 ◽  
Mammalian Genome ◽  
Chromatin Region ◽  
Histone H3 Acetylation ◽  
Transcription Activators ◽  
And Function ◽  
H3 Acetylation

ABSTRACT Histone modifications are associated with distinct transcription states and serve as heritable epigenetic markers for chromatin structure and function. While H3 K9 methylation defines condensed heterochromatin that is able to silence a nearby gene, how gene silencing within euchromatin regions is achieved remains elusive. We report here that histone H3 K4 methylation or K9/K14 acetylation defines distinct chromatin regions permissive or nonpermissive for transgene expression. A permissive chromatin region is enriched in H3 K4 methylation and H3 acetylation, while a nonpermissive region is poor in or depleted of these two histone modifications. The histone modification states of the permissive chromatin can spread to transgenic promoters. However, de novo histone H3 acetylation and H3 K4 methylation at a transgenic promoter in a nonpermissive chromatin region are stochastic, leading to variegated transgene expression. Moreover, nonpermissive chromatin progressively silences a transgene, an event that is accompanied by the reduction of H3 K4 methylation and H3 acetylation levels at the transgenic promoter. These repressive effects of nonpermissive chromatin cannot be completely countered by strong transcription activators, indicating the dominance of the chromatin effects. We therefore propose a model in which histone H3 acetylation and H3 K4 methylation localized to discrete sites in the mammalian genome mark distinct chromatin functions that dictate transgene expression or silencing.

scholarly journals DNaseI‐hypersensitivity and qRT‐PCR analysis of a chromatin region linked to FSH muscular dystrophy

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
KOJI TSUMAGARI ◽  
Xueqiung Xu ◽  
Greg Crawford ◽  
Melanie Ehrlich
Keyword(s):  
Muscular Dystrophy ◽  
Pcr Analysis ◽  
Chromatin Region ◽  
Qrt Pcr

scholarly journals Aurora A Phosphorylates MCAK to Control Ran-dependent Spindle Bipolarity

2008 ◽  
Vol 19 (7) ◽  
pp. 2752-2765 ◽  
Author(s):  
Xin Zhang ◽  
Stephanie C. Ems-McClung ◽  
Claire E. Walczak
Keyword(s):  
Phosphorylation Site ◽  
Aurora B ◽  
Aurora A ◽  
Spindle Formation ◽  
Chromatin Region ◽  
Spindle Poles ◽  
Egg Extracts ◽  
Xenopus Egg ◽  
Xenopus Egg Extracts ◽  
Bipolar Spindles

During mitosis, mitotic centromere-associated kinesin (MCAK) localizes to chromatin/kinetochores, a cytoplasmic pool, and spindle poles. Its localization and activity in the chromatin region are regulated by Aurora B kinase; however, how the cytoplasmic- and pole-localized MCAK are regulated is currently not clear. In this study, we used Xenopus egg extracts to form spindles in the absence of chromatin and centrosomes and found that MCAK localization and activity are tightly regulated by Aurora A. This regulation is important to focus microtubules at aster centers and to facilitate the transition from asters to bipolar spindles. In particular, we found that MCAK colocalized with NuMA and XMAP215 at the center of Ran asters where its activity is regulated by Aurora A-dependent phosphorylation of S196, which contributes to proper pole focusing. In addition, we found that MCAK localization at spindle poles was regulated through another Aurora A phosphorylation site (S719), which positively enhances bipolar spindle formation. This is the first study that clearly defines a role for MCAK at the spindle poles as well as identifies another key Aurora A substrate that contributes to spindle bipolarity.

scholarly journals Nup2 requires a highly divergent partner, NupA, to fulfill functions at nuclear pore complexes and the mitotic chromatin region

2015 ◽  
Vol 26 (4) ◽  
pp. 605-621 ◽  
Author(s):  
Sarine Markossian ◽  
Subbulakshmi Suresh ◽  
Aysha H. Osmani ◽  
Stephen A. Osmani
Keyword(s):  
Spindle Assembly Checkpoint ◽  
Ectopic Expression ◽  
Nuclear Pore ◽  
Nuclear Pore Complexes ◽  
Chromatin Region ◽  
Mitotic Kinase ◽  
Pore Complexes ◽  
Surveillance Mechanism ◽  
Insight Into ◽  
Mitotic Chromatin

Chromatin and nuclear pore complexes (NPCs) undergo dramatic changes during mitosis, which in vertebrates and Aspergillus nidulans involves movement of Nup2 from NPCs to the chromatin region to fulfill unknown functions. This transition is shown to require the Cdk1 mitotic kinase and be promoted prematurely by ectopic expression of the NIMA kinase. Nup2 localizes with a copurifying partner termed NupA, a highly divergent yet essential NPC protein. NupA and Nup2 locate throughout the chromatin region during prophase but during anaphase move to surround segregating DNA. NupA function is shown to involve targeting Nup2 to its interphase and mitotic locations. Deletion of either Nup2 or NupA causes identical mitotic defects that initiate a spindle assembly checkpoint (SAC)–dependent mitotic delay and also cause defects in karyokinesis. These mitotic problems are not caused by overall defects in mitotic NPC disassembly–reassembly or general nuclear import. However, without Nup2 or NupA, although the SAC protein Mad1 locates to its mitotic locations, it fails to locate to NPCs normally in G1 after mitosis. Collectively the study provides new insight into the roles of Nup2 and NupA during mitosis and in a surveillance mechanism that regulates nucleokinesis when mitotic defects occur after SAC fulfillment.

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