Faculty Opinions recommendation of A bacterial effector acts as a plant transcription factor and induces a cell size regulator.

Pathogenicity of many Gram-negative bacteria relies on the injection of effector proteins by type III secretion into eukaryotic cells, where they modulate host signaling pathways to the pathogen's benefit. One such effector protein injected by Xanthomonas into plants is AvrBs3, which localizes to the plant cell nucleus and causes hypertrophy of plant mesophyll cells. We show that AvrBs3 induces the expression of a master regulator of cell size, upa20, which encodes a transcription factor containing a basic helix-loop-helix domain. AvrBs3 binds to a conserved element in the upa20 promoter via its central repeat region and induces gene expression through its activation domain. Thus, AvrBs3 and likely other members of this family provoke developmental reprogramming of host cells by mimicking eukaryotic transcription factors.

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Spindle scaling mechanisms

Essays in Biochemistry ◽

10.1042/ebc20190064 ◽

2020 ◽

Vol 64 (2) ◽

pp. 383-396

Author(s):

Lara K. Krüger ◽

Phong T. Tran

Keyword(s):

Cell Size ◽

Spindle Assembly ◽

Dependent Manner ◽

Post Translational Modification ◽

Size Dependent ◽

A Cell ◽

Chromosome Separation ◽

Spindle Elongation ◽

Protein Gradients ◽

Spindle Structure

Abstract The mitotic spindle robustly scales with cell size in a plethora of different organisms. During development and throughout evolution, the spindle adjusts to cell size in metazoans and yeast in order to ensure faithful chromosome separation. Spindle adjustment to cell size occurs by the scaling of spindle length, spindle shape and the velocity of spindle assembly and elongation. Different mechanisms, depending on spindle structure and organism, account for these scaling relationships. The limited availability of critical spindle components, protein gradients, sequestration of spindle components, or post-translational modification and differential expression levels have been implicated in the regulation of spindle length and the spindle assembly/elongation velocity in a cell size-dependent manner. In this review, we will discuss the phenomenon and mechanisms of spindle length, spindle shape and spindle elongation velocity scaling with cell size.

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Emulsion flow which preparation excludes a presence of mechanical impurities

Proceedings of the Mavlyutov Institute of Mechanics ◽

10.21662/uim2012.2.061 ◽

2012 ◽

Vol 9 (2) ◽

pp. 118-122

Author(s):

A.A. Rakhimov

Keyword(s):

Cell Size ◽

First Case ◽

A Cell ◽

Emulsion Flow ◽

Blocking Mechanism

Experiments were carried out with waterhydrocarbon emulsions with various emulsifiers in capillaries with a length of 2 cm, diameters of 40 and 100 µm. To eliminate the influence of mechanical impurities comparable in size with the diameter of the capillary in first case emulsion components were filtered through fine-meshed filters. In second case obtained that way emulsion was additionally filtered through a system consisting of 3 filters with a cell size of 30-40 microns. In a capillary of 100 µm such emulsion came in a blocked state. Additional filtration of the emulsion through the mesh filters have led to an increase in viscosity but in 100 µm capillaries the time until the blocking 2-3 times more than the original. Rheology of used emulsions is well described by the model of Ostwald-de Waale. It was determined that emulsion blocking mechanism is due to the presence of inclusions not emulsion viscosity.

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Syntaxin 1A Gene Is Negatively Regulated in a Cell/Tissue Specific Manner by YY1 Transcription Factor, Which Binds to the −183 to −137 Promoter Region Together with Gene Silencing Factors Including Histone Deacetylase

Biomolecules ◽

10.3390/biom11020146 ◽

2021 ◽

Vol 11 (2) ◽

pp. 146

Author(s):

Takahiro Nakayama ◽

Toshiyuki Fukutomi ◽

Yasuo Terao ◽

Kimio Akagawa

Keyword(s):

Transcription Factor ◽

Gene Silencing ◽

Protein Complex ◽

Promoter Region ◽

Neuronal Cell ◽

Syntaxin 1A ◽

Tissue Specific ◽

Cell Tissue ◽

Specific Manner ◽

A Cell

The HPC-1/syntaxin 1A (Stx1a) gene, which is involved in synaptic transmission and neurodevelopmental disorders, is a TATA-less gene with several transcription start sites. It is activated by the binding of Sp1 and acetylated histone H3 to the −204 to +2 core promoter region (CPR) in neuronal cell/tissue. Furthermore, it is depressed by the association of class 1 histone deacetylases (HDACs) to Stx1a–CPR in non-neuronal cell/tissue. To further clarify the factors characterizing Stx1a gene silencing in non-neuronal cell/tissue not expressing Stx1a, we attempted to identify the promoter region forming DNA–protein complex only in non-neuronal cells. Electrophoresis mobility shift assays (EMSA) demonstrated that the −183 to −137 OL2 promoter region forms DNA–protein complex only in non-neuronal fetal rat skin keratinocyte (FRSK) cells which do not express Stx1a. Furthermore, the Yin-Yang 1 (YY1) transcription factor binds to the −183 to −137 promoter region of Stx1a in FRSK cells, as shown by competitive EMSA and supershift assay. Chromatin immunoprecipitation assay revealed that YY1 in vivo associates to Stx1a–CPR in cell/tissue not expressing Stx1a and that trichostatin A treatment in FRSK cells decreases the high-level association of YY1 to Stx1a-CPR in default. Reporter assay indicated that YY1 negatively regulates Stx1a transcription. Finally, mass spectrometry analysis showed that gene silencing factors, including HDAC1, associate onto the −183 to −137 promoter region together with YY1. The current study is the first to report that Stx1a transcription is negatively regulated in a cell/tissue-specific manner by YY1 transcription factor, which binds to the −183 to −137 promoter region together with gene silencing factors, including HDAC.

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A Banana PHD-Type Transcription Factor MaPHD1 Represses a Cell Wall-Degradation Gene MaXTH6 during Fruit Ripening

Horticultural Plant Journal ◽

10.1016/j.hpj.2017.08.003 ◽

2017 ◽

Vol 3 (5) ◽

pp. 190-198 ◽

Cited By ~ 2

Author(s):

Wei WEI ◽

Zhongqi FAN ◽

Jianye CHEN ◽

Jianfei KUANG ◽

Wangjin LU ◽

...

Keyword(s):

Cell Wall ◽

Transcription Factor ◽

Fruit Ripening ◽

Cell Wall Degradation ◽

A Cell

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A Cell-Permeable Synthetic Transcription Factor Mimic

Angewandte Chemie International Edition ◽

10.1002/anie.200604485 ◽

2007 ◽

Vol 46 (16) ◽

pp. 2865-2868 ◽

Cited By ~ 58

Author(s):

Xiangshu Xiao ◽

Peng Yu ◽

Hyun-Suk Lim ◽

Devanjan Sikder ◽

Thomas Kodadek

Keyword(s):

Transcription Factor ◽

A Cell

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Growth in cell length in the fission yeast Schizosaccharomyces pombe

Journal of Cell Science ◽

10.1242/jcs.75.1.357 ◽

1985 ◽

Vol 75 (1) ◽

pp. 357-376 ◽

Cited By ~ 2

Author(s):

J.M. Mitchison ◽

P. Nurse

Keyword(s):

Schizosaccharomyces Pombe ◽

Cell Size ◽

Single Cells ◽

Temperature Shift ◽

Time Lapse ◽

Cell Length ◽

Wild Type ◽

Cycle Growth ◽

A Cell ◽

Mutant Cells

The cylindrical cells of Schizosaccharomyces pombe grow in length by extension at the ends and not the middle. At the beginning of the cell cycle, growth is restricted to the ‘old end’, which existed in the previous cycle. Later on, the ‘new end’, formed from the septum, starts to grow at a point in the cycle that we have called NETO (‘new end take-off’). Fluorescence microscopy on cells stained with Calcofluor has been used to study NETO in size mutants, in blocked cdc mutants and with different growth temperatures and media. In wild-type cells (strain 972) NETO happens at 0.34 of the cycle with a cell length of 9.5 microns. With size mutants that are smaller at division, NETO takes place at the same size (9.0-9.5 microns) but this is not achieved until later in the cycle. Another control operates in larger size mutants since NETO occurs at the same stage of the cycle (about 0.32) as in wild type but at a larger cell size. This control is probably a requirement to have completed an event in early G2, since most cdc mutant cells blocked before this point in the cycle do not show NETO whereas most of those blocked in late G2 do show it. We conclude that NETO only happens if: (1) the cell length is greater than a critical value of 9.0-9.5 microns; and (2) the cell has traversed the first 0.3-0.35 of the cycle and passed early G2. NETO is delayed in poor media, in which cell size is also reduced. Temperature has little effect on NETO under steady-state conditions, but there is a transient delay for some hours after a temperature shift. NETO is later in another wild-type strain, 132. Time-lapse photomicrography was used to follow the rates of length growth in single cells. Wild-type cells showed two linear segments during the first 75% of the cycle. There was a rate-change point (RCP), coincident with NETO, where the rate of total length extension increased by 35%. This increase was not due simply to the start of new-end growth, since old-end growth slowed down in some cells at the RCP. cdc 11.123 is a mutant in which septation and division is blocked at 35 degrees C but nuclear division continues.(ABSTRACT TRUNCATED AT 400 WORDS)

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Abstract 643: Type-2 Cannabinoid Receptor Deficiency is Associated with Atherosclerotic Lesion Calcification in Ldlr-null Mice

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.36.suppl_1.643 ◽

2016 ◽

Vol 36 (suppl_1) ◽

Author(s):

Makenzie L Fulmer ◽

Emilee Englehaupt ◽

Chris Garst ◽

Stacy Brown ◽

Douglas Thewke

Keyword(s):

Transcription Factor ◽

Cannabinoid Receptor ◽

Atherosclerotic Lesion ◽

Increased Risk ◽

Calcified Plaque ◽

En Face ◽

Related Transcription Factor ◽

A Cell ◽

Complex Signaling

Background: Calcification of atherosclerotic plaques is associated with vulnerability to rupture and increased risk of myocardial infarction. The mechanism of plaque calcification is unclear, but has been shown to be a cell-mediated process involving complex signaling pathways affecting the osteogenic transcription factor Runt-related transcription factor 2 (Runx2). The type-2 cannabinoid receptor (CB2) modulates processes involved in bone remodeling and our prior studies determined that CB2 alters the composition of early lesions in hyperlipidemic Ldlr -/- mice; however, the function of CB2 in plaque calcification is unknown. Therefore, we tested the hypothesis that CB2 modulates plaque calcification by evaluating the effects of systemic CB2 gene deletion on lesion calcification and aortic expression of Runx2 in Ldlr -/- mice. Results: Groups (n≥8) of 8-week old CB2 +/+ Ldlr -/- (WT) and CB2 -/- Ldlr -/- (CB2 -/- ) mice were fed a high fat diet (HFD) for up to 24 weeks. Standard blood plasma analysis showed no difference in HFD-induced hyperlipidemia between WT and CB2 -/- mice. Aortic levels of endocannabinoids, anandamide and 2-archidonylglycerol, were significantly elevated after 12 weeks of HFD feeding as determined by LC-MS/MS. En face analysis revealed the extent of atherosclerosis in the aortic arch and thoracic aorta did not differ between WT and CB2 -/- mice, but was ~1.9-fold greater in the abdominal aortas of CB2 -/- mice (17.0±1.3% vs 9.0±1.3%, p=0.002). Calcification of aortic root lesions was ~2.3 fold greater in CB2 -/- mice compared to WT mice (12.9±1.1% vs 5.6±1.2%, p=0.002) as revealed by von Kossa staining. Western blot analysis showed significantly increased expression of Runx2 in aortas of WT mice compared to CB2 -/- after 20 weeks of HFD (2.55±0.25 fold, p<0.05). Conclusion: Systemic CB2 deficiency enhances lesion calcification and is associated with altered aortic expression of Runx2. These results provide novel mechanistic insights into the function of CB2 signaling in the pathogenesis of atherosclerosis and vascular calcification that may lead to the development of therapies aimed at stabilizing calcified plaque.

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