scholarly journals Prospects for enhancing leaf photosynthetic capacity by manipulating mesophyll cell morphology

2018 ◽  
Author(s):  
Tao Ren ◽  
Sarathi M Weraduwage ◽  
Thomas D. Sharkey
Keyword(s):  
Cell Morphology ◽  
Leaf Anatomy ◽  
Target Genes ◽  
Photosynthetic Capacity ◽  
Control Cell ◽  
Mesophyll Cell ◽  
Light Distribution ◽  
Potential Target ◽  
Unit Leaf ◽  
Physiological Processes

AbstractLeaves are beautifully specialized organs designed to maximize the use of light and CO2 for photosynthesis. Engineering leaf anatomy therefore brings great potential to enhance photosynthetic capacity. Here we review the effect of the dominant leaf anatomical traits on leaf photosynthesis and confirm that a high chloroplast surface area exposed to intercellular airspace per unit leaf area (Sc) is critical for efficient photosynthesis. The possibility of improving Sc through appropriately increasing mesophyll cell density is further analyzed. The potential influences of modifying mesophyll cell morphology on CO2 diffusion, light distribution within the leaf, and other physiological processes are also discussed. Some potential target genes regulating leaf mesophyll cell proliferation and expansion are explored. Indeed, more comprehensive research is needed to understand how manipulating mesophyll cell morphology through editing the potential target genes impact leaf photosynthetic capacity and related physiological processes. This will pinpoint the targets for engineering leaf anatomy to maximize photosynthetic capacity.HighlightCell morphology in leaves affects photosynthesis by controlling CO2 diffusion and light distribution. Recent work has uncovered genes that control cell size, shape, and number paving the way improved photosynthesis.

scholarly journals Prospects for enhancing leaf photosynthetic capacity by manipulating mesophyll cell morphology

2018 ◽  
Vol 70 (4) ◽  
pp. 1153-1165 ◽  
Author(s):  
Tao Ren ◽  
Sarathi M Weraduwage ◽  
Thomas D Sharkey
Keyword(s):  
Cell Morphology ◽  
Photosynthetic Capacity ◽  
Mesophyll Cell

scholarly journals Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer

2021 ◽  
Author(s):  
Chun Yang ◽  
Stéphane Croteau ◽  
Pierre Hardy
Keyword(s):  
Histone Deacetylase ◽  
Posttranslational Modifications ◽  
Histone Deacetylases ◽  
Muscle Development ◽  
Target Genes ◽  
Human Cancer ◽  
Expression Patterns ◽  
Aberrant Expression ◽  
Physiological Processes ◽  
Cancer Pathogenesis

Abstract Background HDAC9 (histone deacetylase 9) belongs to the class IIa family of histone deacetylases. This enzyme can shuttle freely between the nucleus and cytoplasm and promotes tissue-specific transcriptional regulation by interacting with histone and non-histone substrates. HDAC9 plays an essential role in diverse physiological processes including cardiac muscle development, bone formation, adipocyte differentiation and innate immunity. HDAC9 inhibition or activation is therefore a promising avenue for therapeutic intervention in several diseases. HDAC9 overexpression is also common in cancer cells, where HDAC9 alters the expression and activity of numerous relevant proteins involved in carcinogenesis. Conclusions This review summarizes the most recent discoveries regarding HDAC9 as a crucial regulator of specific physiological systems and, more importantly, highlights the diverse spectrum of HDAC9-mediated posttranslational modifications and their contributions to cancer pathogenesis. HDAC9 is a potential novel therapeutic target, and the restoration of aberrant expression patterns observed among HDAC9 target genes and their related signaling pathways may provide opportunities to the design of novel anticancer therapeutic strategies.

scholarly journals PPARgene: A Database of Experimentally Verified and Computationally Predicted PPAR Target Genes

PPAR Research ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Li Fang ◽  
Man Zhang ◽  
Yanhui Li ◽  
Yan Liu ◽  
Qinghua Cui ◽  
...  
Keyword(s):  
In Silico ◽  
Target Gene ◽  
Target Genes ◽  
Prediction Method ◽  
Peroxisome Proliferator ◽  
Physiological Processes ◽  
Peroxisome Proliferator Activated Receptors ◽  
High Throughput Gene Expression ◽  
Responsive Element ◽  
Target Gene Transcription

The peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors of the nuclear receptor superfamily. Upon ligand binding, PPARs activate target gene transcription and regulate a variety of important physiological processes such as lipid metabolism, inflammation, and wound healing. Here, we describe the first database of PPAR target genes, PPARgene. Among the 225 experimentally verified PPAR target genes, 83 are for PPARα, 83 are for PPARβ/δ, and 104 are for PPARγ. Detailed information including tissue types, species, and reference PubMed IDs was also provided. In addition, we developed a machine learning method to predict novel PPAR target genes by integratingin silicoPPAR-responsive element (PPRE) analysis with high throughput gene expression data. Fivefold cross validation showed that the performance of this prediction method was significantly improved compared to thein silicoPPRE analysis method. The prediction tool is also implemented in the PPARgene database.

scholarly journals Proposed megakaryocytic regulon of p53: the genes engaged to control cell cycle and apoptosis during megakaryocytic differentiation

2012 ◽  
Vol 44 (12) ◽  
pp. 638-650 ◽  
Author(s):  
Pani A. Apostolidis ◽  
Stephan Lindsey ◽  
William M. Miller ◽  
Eleftherios T. Papoutsakis
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Cell Line ◽  
Target Genes ◽  
Control Cell ◽  
P53 Expression ◽  
Megakaryocytic Differentiation ◽  
Knock Down ◽  
Cell Cycling ◽  
And Control

During endomitosis, megakaryocytes undergo several rounds of DNA synthesis without division leading to polyploidization. In primary megakaryocytes and in the megakaryocytic cell line CHRF, loss or knock-down of p53 enhances cell cycling and inhibits apoptosis, leading to increased polyploidization. To support the hypothesis that p53 suppresses megakaryocytic polyploidization, we show that stable expression of wild-type p53 in K562 cells (a p53-null cell line) attenuates the cells' ability to undergo polyploidization during megakaryocytic differentiation due to diminished DNA synthesis and greater apoptosis. This suggested that p53's effects during megakaryopoiesis are mediated through cell cycle- and apoptosis-related target genes, possibly by arresting DNA synthesis and promoting apoptosis. To identify candidate genes through which p53 mediates these effects, gene expression was compared between p53 knock-down (p53-KD) and control CHRF cells induced to undergo terminal megakaryocytic differentiation using microarray analysis. Among substantially downregulated p53 targets in p53-KD megakaryocytes were cell cycle regulators CDKN1A (p21) and PLK2, proapoptotic FAS, TNFRSF10B, CASP8, NOTCH1, TP53INP1, TP53I3, DRAM1, ZMAT3 and PHLDA3, DNA-damage-related RRM2B and SESN1, and actin component ACTA2, while antiapoptotic CKS1B, BCL2, GTSE1, and p53 family member TP63 were upregulated in p53-KD cells. Additionally, a number of cell cycle-related, proapoptotic, and cytoskeleton-related genes with known functions in megakaryocytes but not known to carry p53-responsive elements were differentially expressed between p53-KD and control CHRF cells. Our data support a model whereby p53 expression during megakaryopoiesis serves to control polyploidization and the transition from endomitosis to apoptosis by impeding cell cycling and promoting apoptosis. Furthermore, we identify a putative p53 regulon that is proposed to orchestrate these effects.

scholarly journals Identification of potential target genes of USP22 via ChIP-seq and RNA-seq analysis in HeLa cells

2018 ◽  
Vol 41 (2) ◽  
pp. 488-495 ◽  
Author(s):  
Zhen Gong ◽  
Jianyun Liu ◽  
Xin Xie ◽  
Xiaoyuan Xu ◽  
Ping Wu ◽  
...  
Keyword(s):  
Hela Cells ◽  
Target Genes ◽  
Rna Seq ◽  
Potential Target

Elevation of MicroRNA-126 Levels in Intracranial Aneurysm and Bioinformatic Analysis of Potential Molecular Mechanisms

2021 ◽  
Vol 11 (4) ◽  
pp. 573-579
Author(s):  
Pan Huang ◽  
Min Xu ◽  
Xiao-Ying He
Keyword(s):  
Intracranial Aneurysm ◽  
Peripheral Blood ◽  
Target Gene ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Kegg Pathway ◽  
Bioinformatic Analysis ◽  
Control Group ◽  
Potential Target ◽  
Fas Signaling

The study is to investigation of microRNA-126 levels in patients with intracranial aneurysm and bioinformatic analysis of the molecular mechanisms involved. A total of 166 patients with ICA who were hospitalized or examined in our hospital from September 2015 to December 2017 were used as the experimental group (ICA group). This group included 120 patients with unruptured intracranial aneurysm (UICA; UICA group) and 46 patients with ruptured intracranial aneurysm (RICA); RICA group). The UICA group was further subdivided into 42 surgical groups (S group) and 78 nonsurgical groups (NS group). Sixty-three normal people without intracranial aneurysms were selected as the control group. RT-PCR was used to quantitatively detect the relative expression of microRNA- 126 in peripheral blood mononuclear cells at the time of admission and immediately after surgery. The UCSC database was used to analyze the gene locus and homology of microRNA-126. The TargetScan database and CoMeTa database were used to predict the potential target genes of microRNA-126. The DAVID database was used to enrich the function of potential target genes of microRNA-126 (GO enrichment) and KEGG pathway enrichment for analysis. The expression level of microRNA-126 in peripheral blood was significantly higher in the ICA group than in the control group (P <0.01), significantly higher in the RICA group than in the UICA group (P <0.05). Expression was also higher in the NS group than in the S group but the difference was nonsignificant (P >0.05). A total of 15 potential target genes including ITGA6, CRK, PCDH7, and ADAM9 were identified through the target gene prediction software and GO analysis and KEGG pathway analysis showed that the function of the microRNA-126 target gene was mainly focused on protein binding and the FAS signaling pathway. In Conclusion the microRNA-126 is up-regulated in ICA patients and affects ICA by regulating multiple target genes in the FAS signaling pathway.

scholarly journals miR-615 Fine-Tunes Growth and Development and Has a Role in Cancer and in Neural Repair

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1566 ◽  
Author(s):  
Marisol Godínez-Rubí ◽  
Daniel Ortuño-Sahagún
Keyword(s):  
Growth And Development ◽  
Target Genes ◽  
Noncoding Rnas ◽  
Tumor Promoter ◽  
Neural Repair ◽  
Small Noncoding Rnas ◽  
Physiological Processes ◽  
And Migration ◽  
Migration Of Cells ◽  
Regulation Of Growth

MicroRNAs (miRNAs) are small noncoding RNAs that function as epigenetic modulators regulating almost any gene expression. Similarly, other noncoding RNAs, as well as epigenetic modifications, can regulate miRNAs. This reciprocal interaction forms a miRNA-epigenetic feedback loop, the deregulation of which affects physiological processes and contributes to a great diversity of diseases. In the present review, we focus on miR-615, a miRNA highly conserved across eutherian mammals. It is involved not only during embryogenesis in the regulation of growth and development, for instance during osteogenesis and angiogenesis, but also in the regulation of cell growth and the proliferation and migration of cells, acting as a tumor suppressor or tumor promoter. It therefore serves as a biomarker for several types of cancer, and recently has also been found to be involved in reparative processes and neural repair. In addition, we present the pleiad of functions in which miR-615 is involved, as well as their multiple target genes and the multiple regulatory molecules involved in its own expression. We do this by introducing in a comprehensible way the reported knowledge of their actions and interactions and proposing an integral view of its regulatory mechanisms.

scholarly journals Leaf Removal Affects Maize Morphology and Grain Yield

Agronomy ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 269 ◽  
Author(s):  
Guangzhou Liu ◽  
Yunshan Yang ◽  
Wanmao Liu ◽  
Xiaoxia Guo ◽  
Jun Xue ◽  
...  
Keyword(s):  
Grain Yield ◽  
Leaf Area ◽  
Field Experiments ◽  
Photosynthetic Capacity ◽  
Maize Yield ◽  
Light Distribution ◽  
Planting Density ◽  
Leaf Removal ◽  
Area Index ◽  
Source Sink

Increasing planting density is an important practice associated with increases in maize yield, but densely planted maize can suffer from poor light conditions. In our two-year field experiments, two morphologically different cultivars, ZD958 (less compact) and DH618 (more compact), were planted at 120,000 plants ha−1 and 135,000 plants ha−1, respectively. We established different leaf area index (LAI) treatments by removing leaves three days after silking: (1) control, no leaves removed (D0); (2) the two uppermost leaves removed (D1); (3) the four uppermost leaves removed (D2); (4) the leaves below the third leaf below the ear removed (D3); (5) the leaves of D1 and D3 removed (D4); (6) the leaves of D2 and D3 removed (D5). Optimal leaf removal improved light distribution, increased photosynthetic capacity and the post-silking source-sink ratio, and thus the grain yield, with an average LAI of 5.9 (5.6 and 6.2 for ZD958 and DH618, respectively) for the highest yields in each year. Therefore, less-compact cultivars should have smaller or fewer topmost leaves or leaves below the ear that quickly senesce post-silking, so as to decrease leaf area and thus improve light distribution and photosynthetic capacity in the canopy under dense planting conditions. However, for more compact cultivars, leaves below the ear should senesce quickly after silking to reduce leaf respiration and improve the photosynthetic capacity of the remaining top residual leaves. In future maize cultivation, compact cultivars with optimal post-silking LAI should be adopted when planting densely.

scholarly journals Role of co-regulators in metabolic and transcriptional actions of thyroid hormone

2016 ◽  
Vol 56 (3) ◽  
pp. R73-R97 ◽  
Author(s):  
Inna Astapova
Keyword(s):  
Thyroid Hormone ◽  
Transcriptional Repression ◽  
Target Genes ◽  
Thyroid Hormone Receptor ◽  
Retinoic Acid Receptor ◽  
Specific Response ◽  
Physiological Processes ◽  
Genome Wide ◽  
Wide Range ◽  
And Function

Thyroid hormone (TH) controls a wide range of physiological processes through TH receptor (TR) isoforms. Classically, TRs are proposed to function as tri-iodothyronine (T3)-dependent transcription factors: on positively regulated target genes, unliganded TRs mediate transcriptional repression through recruitment of co-repressor complexes, while T3binding leads to dismissal of co-repressors and recruitment of co-activators to activate transcription. Co-repressors and co-activators were proposed to play opposite roles in the regulation of negative T3target genes and hypothalamic–pituitary–thyroid axis, but exact mechanisms of the negative regulation by TH have remained elusive. Important insights into the roles of co-repressors and co-activators in different physiological processes have been obtained using animal models with disrupted co-regulator function. At the same time, recent studies interrogating genome-wide TR binding have generated compelling new data regarding effects of T3, local chromatin structure, and specific response element configuration on TR recruitment and function leading to the proposal of new models of transcriptional regulation by TRs. This review discusses data obtained in various mouse models with manipulated function of nuclear receptor co-repressor (NCoR or NCOR1) and silencing mediator of retinoic acid receptor and thyroid hormone receptor (SMRT or NCOR2), and family of steroid receptor co-activators (SRCs also known as NCOAs) in the context of TH action, as well as insights into the function of co-regulators that may emerge from the genome-wide TR recruitment analysis.

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