scholarly journals Light involved regulation of BZR1 stability and phosphorylation status to coordinate plant growth in Arabidopsis

2017 ◽  
Vol 37 (2) ◽  
Author(s):  
Qian-Feng Li ◽  
Li-Chun Huang ◽  
Ke Wei ◽  
Jia-Wen Yu ◽  
Chang-Quan Zhang ◽  
...  
Keyword(s):  
Plant Growth ◽  
Molecular Mechanisms ◽  
Protein Biosynthesis ◽  
Transcript Abundance ◽  
26S Proteasome ◽  
Gene Encoding ◽  
Regulation Network ◽  
Phosphatase 2A ◽  
Integration Node ◽  
Proteasome Pathway

Light and brassinosteroid (BR) are master environmental stimulus and endogenous cue for plant growth and development respectively. Great progress has been made in elucidating the molecular mechanisms on the cross-talk between light and BR. However, little is known about how BZR1, the pivotal integration node, is regulated by light and dark. Here, we demonstrated that an intact BR signaling pathway is essential for dark-induced hypocotyl elongation. Consequent expression assay showed that light–dark switch affected BZR1 phosphorylation and accumulation. Moreover, blocking the 26S proteasome pathway promoted the accumulation of both phosphorylated and dephosphorylated BZR1 proteins. Restriction of new protein biosynthesis had multiple effects on BZR1 phosphorylation status and stability, relying on the availability of light and the 26S proteasome pathways. Furthermore, sugar treatment strikingly enhanced the accumulation of total BZR1 under either light or dark conditions, likely by repressing transcript abundance of MAX2, a gene encoding an E3 ligase for BZR1. Finally, light-regulated phosphorylation change of BZR1 requires the existence of endogenous BR as well as functional BIN2 and protein phosphatase 2A (PP2A). Taken together, our results depicted a light-involved complex regulation network of BZR1 stability and phosphorylation status.

scholarly journals OseIF3h Regulates Plant Growth and Pollen Development at Translational Level Presumably through Interaction with OsMTA2

Plants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1101
Author(s):  
Yuqing Huang ◽  
Peng Zheng ◽  
Xuejiao Liu ◽  
Hao Chen ◽  
Jumin Tu
Keyword(s):  
Plant Growth ◽  
Translation Initiation ◽  
Pollen Development ◽  
Messenger Rna ◽  
Protein Biosynthesis ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Sequencing Data ◽  
Knock Out ◽  
Translational Level

The initiation stage of protein biosynthesis is a sophisticated process tightly regulated by numerous initiation factors and their associated components. However, the mechanism underlying translation initiation has not been completely understood in rice. Here, we showed knock-out mutation of the rice eukaryotic translation initiation factor 3 subunit h (OseIF3h) resulted in plant growth retardation and seed-setting rate reduction as compared to the wild type. Further investigation demonstrated an interaction between OseIF3h and OsMTA2 (mRNA adenosine methylase 2), a rice homolog of METTL3 (methyltransferase-like 3) in mammals, which provided new insight into how N6-methyladenosine (m6A) modification of messenger RNA (mRNA) is engaged in the translation initiation process in monocot species. Moreover, the RIP-seq (RNA immunoprecipitation sequencing) data suggested that OseIF3h was involved in multiple biological processes, including photosynthesis, cellular metabolic process, precursor metabolites, and energy generation. Therefore, we infer that OseIF3h interacts with OsMTA2 to target a particular subset of genes at translational level, regulating plant growth and pollen development.

scholarly journals Interrogating Plant-Microbe Interactions with Chemical Tools: Click Chemistry Reagents for Metabolic Labeling and Activity-Based Probes

Molecules ◽  
2021 ◽  
Vol 26 (1) ◽  
pp. 243
Author(s):  
Vivian S. Lin
Keyword(s):  
Plant Growth ◽  
Immune Responses ◽  
Click Chemistry ◽  
Chemical Biology ◽  
Molecular Mechanisms ◽  
Metabolic Labeling ◽  
Beneficial Microbes ◽  
Plant Hosts ◽  
Microbe Interactions ◽  
Growth Metabolism

Continued expansion of the chemical biology toolbox presents many new and diverse opportunities to interrogate the fundamental molecular mechanisms driving complex plant–microbe interactions. This review will examine metabolic labeling with click chemistry reagents and activity-based probes for investigating the impacts of plant-associated microbes on plant growth, metabolism, and immune responses. While the majority of the studies reviewed here used chemical biology approaches to examine the effects of pathogens on plants, chemical biology will also be invaluable in future efforts to investigate mutualistic associations between beneficial microbes and their plant hosts.

Stable transfer and restricted expression of a cloned class I gene encoding a secreted transplantation-like antigen

1985 ◽  
Vol 5 (6) ◽  
pp. 1295-1300
Author(s):  
Y Barra ◽  
K Tanaka ◽  
K J Isselbacher ◽  
G Khoury ◽  
G Jay
Keyword(s):  
Molecular Mechanisms ◽  
Cell Types ◽  
Class I ◽  
Regulatory Sequences ◽  
Transcriptional Enhancer ◽  
Gene Encoding ◽  
Specific Expression ◽  
Tissue Specific ◽  
Functional Studies ◽  
I Gene

The identification of a unique major histocompatibility complex class I gene, designated Q10, which encodes a secreted rather than a cell surface antigen has led to questions regarding its potential role in regulating immunological functions. Since the Q10 gene is specifically activated only in the liver, we sought to define the molecular mechanisms which control its expression in a tissue-specific fashion. Results obtained by transfection of the cloned Q10 gene, either in the absence or presence of a heterologous transcriptional enhancer, into a variety of cell types of different tissue derivations are consistent with the Q10 gene being regulated at two levels. The first is by a cis-dependent mechanism which appears to involve site-specific DNA methylation. The second is by a trans-acting mechanism which would include the possibility of an enhancer binding factor. The ability to efficiently express the Q10 gene in certain transfected cell lines offers an opportunity to obtain this secreted class I antigen in quantities sufficient for functional studies; this should also make it possible to define regulatory sequences which may be responsible for the tissue-specific expression of Q10.

Molecular Insights into Beneficial Effects of Tea-Plant Growth and Selenium Enrichment by Herbaspirillum camelliae

2021 ◽  
pp. 37-51
Author(s):  
Wei Cheng ◽  
Xuejing Yu ◽  
Xingguo Wang
Keyword(s):  
Plant Growth ◽  
Molecular Mechanisms ◽  
Acc Deaminase ◽  
Nitrogen Sources ◽  
Endophytic Bacterium ◽  
Tea Plant ◽  
Nitrogen Fixing ◽  
Biotic And Abiotic Stress ◽  
Bacterial Strains ◽  
Secretion Systems

Herbaspirillum camelliae WT00C, as a tea-plant endophytic bacterium, not only colonizes specifically in tea plants but also promotes tea-plant growth and selenium enrichment. Different from diazotrophic endophytes H. seropedicae, H. frisingense and H. rubrisubalbicans, H. camelliae WT00C does not display nitrogen-fixing activity. To understand the molecular mechanisms of promoting the growth of tea plant and Se-enrichment, we sequenced and annotated the genome of H. camelliae WT00C. The results showed that the genome was composed of 6,079,821 base pairs with a total of 5,537 genes. The genomic survey also revealed that H. camelliae WT00C was a multifunctional bacterium metabolizing a variety of carbon and nitrogen sources and defending against biotic and abiotic stress. Although this bacterium did not have intact nitrogen-fixing genes, its genome held the genes responsible for indole-3-acetic acid (IAA) biosynthesis, 1-aminocyclopropane-1-carboxylate (ACC) deamination, siderophore synthesis, ammonia formation, urea metabolism, glutathione and selenocompound metabolisms. Biosynthesis of IAA, siderophore, ammonia, urea and ACC deaminase could explain why two bacterial strains promote tea-plant growth and development. Selenocompound metabolism in this bacterium might also benefit tea-plant growth and Se-enrichment. In addition, the genome of H. camelliae also contained a multitude of protein secretion systems T1SS, T3SS, T4SS and T6SS, in which T4SS did not exhibit in other members of the genus Herbaspirillum.

Molecular mechanisms of mammalian autophagy

2021 ◽  
Vol 478 (18) ◽  
pp. 3395-3421
Author(s):  
Charles B. Trelford ◽  
Gianni M. Di Guglielmo
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Molecular Pathways ◽  
Zymogen Granules ◽  
Ubiquitin Proteasome Pathway ◽  
Lysine Residues ◽  
Ubiquitin Proteasome ◽  
Proteasome Pathway ◽  
Functional Modulation ◽  
Chaperone Mediated Autophagy

The ubiquitin-proteasome pathway (UPP) and autophagy play integral roles in cellular homeostasis. As part of their normal life cycle, most proteins undergo ubiquitination for some form of redistribution, localization and/or functional modulation. However, ubiquitination is also important to the UPP and several autophagic processes. The UPP is initiated after specific lysine residues of short-lived, damaged or misfolded proteins are conjugated to ubiquitin, which targets these proteins to proteasomes. Autophagy is the endosomal/lysosomal-dependent degradation of organelles, invading microbes, zymogen granules and macromolecules such as protein, carbohydrates and lipids. Autophagy can be broadly separated into three distinct subtypes termed microautophagy, chaperone-mediated autophagy and macroautophagy. Although autophagy was once thought of as non-selective bulk degradation, advancements in the field have led to the discovery of several selective forms of autophagy. Here, we focus on the mechanisms of primary and selective mammalian autophagy pathways and highlight the current knowledge gaps in these molecular pathways.

scholarly journals Transcription of the Human 5-Hydroxytryptamine Receptor 2B (HTR2B) Gene Is under the Regulatory Influence of the Transcription Factors NFI and RUNX1 in Human Uveal Melanoma

2018 ◽  
Vol 19 (10) ◽  
pp. 3272 ◽  
Author(s):  
Manel Benhassine ◽  
Sylvain Guérin
Keyword(s):  
Transcription Factors ◽  
Uveal Melanoma ◽  
Serotonin Receptor ◽  
Molecular Mechanisms ◽  
Regulatory Region ◽  
Gene Signature ◽  
Regulatory Elements ◽  
Gene Encoding ◽  
Aberrant Expression ◽  
Factor I

Because it accounts for 70% of all eye cancers, uveal melanoma (UM) is therefore the most common primary ocular malignancy. In this study, we investigated the molecular mechanisms leading to the aberrant expression of the gene encoding the serotonin receptor 2B (HTR2B), one of the most discriminating among the candidates from the class II gene signature, in metastatic and non-metastatic UM cell lines. Transfection analyses revealed that the upstream regulatory region of the HTR2B gene contains a combination of alternative positive and negative regulatory elements functional in HTR2B− but not in HTR23B+ UM cells. We demonstrated that both the transcription factors nuclear factor I (NFI) and Runt-related transcription factor I (RUNX1) interact with regulatory elements from the HTR2B gene to either activate (NFI) or repress (RUNX1) HTR2B expression in UM cells. The results of this study will help understand better the molecular mechanisms accounting for the abnormal expression of the HTR2B gene in uveal melanoma.

scholarly journals Inversely proportional myelin growth due to altered Pmp22 gene dosage identifies PI3K/Akt/mTOR signaling as a novel therapeutic target in HNPP

2021 ◽  
Author(s):  
Doris Krauter ◽  
David Ewers ◽  
Timon J Hartmann ◽  
Stefan Volkmann ◽  
Theresa Kungl ◽  
...  
Keyword(s):  
Growth Regulation ◽  
Molecular Mechanisms ◽  
Motor Behavior ◽  
Gene Dosage ◽  
Mtor Signaling ◽  
Hereditary Neuropathy ◽  
Gene Encoding ◽  
Phosphatase And Tensin Homolog ◽  
Charcot Marie Tooth Disease ◽  
Tensin Homolog

Duplication of the gene encoding the myelin protein PMP22 causes the hereditary neuropathy Charcot-Marie-Tooth disease 1A (CMT1A), characterized by hypomyelination of medium to large peripheral axons. Conversely, haplo-insufficiency of PMP22 leads to focal myelin overgrowth in hereditary neuropathy with liability to pressure palsies (HNPP). However, the molecular mechanisms of myelin growth regulation by PMP22 remain obscure. Here, we found that the major inhibitor of the myelin growth signaling pathway PI3K/Akt/mTOR, phosphatase and tensin homolog (PTEN) is increased in abundance in CMT1A and decreased in HNPP rodent models. Indeed, treatment of DRG co-cultures from HNPP mice with PI3K/Akt/mTOR pathway inhibitors reduced focal hypermyelination and, importantly, treatment of HNPP mice with the mTOR inhibitor Rapamycin improved motor behavior, increased compound muscle amplitudes (CMAP) and reduced tomacula formation in the peripheral nerve. In Pmp22tg CMT1A mice, we uncovered that the differentiation defect of Schwann cells is independent from PI3K/Akt/mTOR activity, rendering the pathway insufficient as a therapy target on its own. Thus, while CMT1A pathogenesis is governed by dys-differentiation uncoupled from PI3K/Akt/mTOR signaling, targeting the pathway provides novel proof-of-principle for a therapeutic approach to HNPP.

scholarly journals Functions of PPR Proteins in Plant Growth and Development

2021 ◽  
Vol 22 (20) ◽  
pp. 11274
Author(s):  
Xiulan Li ◽  
Mengdi Sun ◽  
Shijuan Liu ◽  
Qian Teng ◽  
Shihui Li ◽  
...  
Keyword(s):  
Plant Growth ◽  
Stress Responses ◽  
Rna Processing ◽  
Growth And Development ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Plant Mitochondria ◽  
Research Progress ◽  
Plant Growth And Development ◽  
Ppr Proteins

Pentatricopeptide repeat (PPR) proteins form a large protein family in land plants, with hundreds of different members in angiosperms. In the last decade, a number of studies have shown that PPR proteins are sequence-specific RNA-binding proteins involved in multiple aspects of plant organellar RNA processing, and perform numerous functions in plants throughout their life cycle. Recently, computational and structural studies have provided new insights into the working mechanisms of PPR proteins in RNA recognition and cytidine deamination. In this review, we summarized the research progress on the functions of PPR proteins in plant growth and development, with a particular focus on their effects on cytoplasmic male sterility, stress responses, and seed development. We also documented the molecular mechanisms of PPR proteins in mediating RNA processing in plant mitochondria and chloroplasts.

Inductive interactions direct early regionalization of the mouse forebrain

Development ◽  
1997 ◽  
Vol 124 (14) ◽  
pp. 2709-2718 ◽  
Author(s):  
K. Shimamura ◽  
J.L. Rubenstein
Keyword(s):  
Sonic Hedgehog ◽  
Bone Morphogenetic Proteins ◽  
Molecular Mechanisms ◽  
Neural Plate ◽  
Gene Encoding ◽  
Prechordal Plate ◽  
Optic Vesicles ◽  
The Central Nervous System ◽  
Anterior Neural Plate ◽  
Anterior Posterior

The cellular and molecular mechanisms that regulate regional specification of the forebrain are largely unknown. We studied the expression of transcription factors in neural plate explants to identify tissues, and the molecules produced by these tissues, that regulate medial-lateral and local patterning of the prosencephalic neural plate. Molecular properties of the medial neural plate are regulated by the prechordal plate perhaps through the action of Sonic Hedgehog. By contrast, gene expression in the lateral neural plate is regulated by non-neural ectoderm and bone morphogenetic proteins. This suggests that the forebrain employs the same medial-lateral (ventral-dorsal) patterning mechanisms present in the rest of the central nervous system. We have also found that the anterior neural ridge regulates patterning of the anterior neural plate, perhaps through a mechanism that is distinct from those that regulate general medial-lateral patterning. The anterior neural ridge is essential for expression of BF1, a gene encoding a transcription factor required for regionalization and growth of the telencephalic and optic vesicles. In addition, the anterior neural ridge expresses Fgf8, and recombinant FGF8 protein is capable of inducing BF1, suggesting that FGF8 regulates the development of anterolateral neural plate derivatives. Furthermore, we provide evidence that the neural plate is subdivided into distinct anterior-posterior domains that have different responses to the inductive signals from the prechordal plate, Sonic Hedgehog, the anterior neural ridge and FGF8. In sum, these results suggest that regionalization of the forebrain primordia is established by several distinct patterning mechanisms: (1) anterior-posterior patterning creates transverse zones with differential competence within the neural plate, (2) patterning along the medial-lateral axis generates longitudinally aligned domains and (3) local inductive interactions, such as a signal(s) from the anterior neural ridge, further define the regional organization.

Abstract MP175: Disruption of the Genome Architecture at the PRRX1 Locus is Associated With the Pathogenesis of LMNA -related Dilated Cardiomyopathy

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Yuan Zhang ◽  
Mohamed Ameen ◽  
Isaac Perea Gil ◽  
Jennifer Arthur ◽  
Alexandra A Gavidia ◽  
...  
Keyword(s):  
Dilated Cardiomyopathy ◽  
Single Cell ◽  
Genome Organization ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Lamin A ◽  
Candidate Locus ◽  
Gene Encoding ◽  
Gene Dysregulation

Background: LMNA , a gene encoding A-type lamin proteins (abbreviated as lamin A), is one of the most frequently mutated genes in dilated cardiomyopathy (DCM). The molecular mechanisms underlying cardiomyocyte dysfunction in LMNA -related DCM remain elusive, translating to the lack of disease-specific therapies. Lamin A has been shown to play a critical role in genome organization via interactions with the chromatin at specific regions called lamina-associated domains (LADs). However, little is known about whether DCM-causing LMNA mutations rearrange the genome conformation and chromosome accessibility. The overarching goal of this study is to define the role of genome organization in LMNA -related DCM. Methods: LMNA -related DCM was modeled in vitro using cardiomyocytes derived from induced pluripotent stem cells (iPSC-CMs) from DCM patients carrying a frameshift mutation in the LMNA gene (c. 348_349insG; p. K117fs) and isogenic controls. We combined genome-wide single cell functional genomic and epigenomic mapping analyses to define the gene regulation and cis-regulatory interactions in isogenic iPSC-CMs. Results: Single-cell RNA-seq revealed global gene dysregulation in LMNA mutant compared to isogenic control iPSC-CMs. The homeodomain transcription factor PRRX1 was significantly upregulated in mutant cells. We showed that LAD integrity is disrupted at the PRRX1 locus in mutant iPSC-CMs. In agreement, DNA fluorescence in situ hybridization (FISH) revealed that the PRRX1 locus loses peripheral association and relocates towards the transcriptionally active nuclear interior in mutant iPSC-CMs. Correspondingly, single-cell assay for transposase accessible chromatin (ATAC)-seq showed increased chromatin co-accessibility at the PRRX1 locus, providing a plausible explanation for ectopic activation of PRRX1 in LMNA mutant iPSC-CMs. Conclusion: Our data suggest that LMNA haploinsufficiency disrupts the structure of LADs, leading to ectopic promoter interactions and altered gene expression in LMNA -related DCM iPSC-CMs. We identified PRRX1 as a promising candidate locus linking changes in LAD organization with gene dysregulation in LMNA -related DCM.

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