scholarly journals Rice LEAFY COTYLEDONE1 regulates embryonic envelope development and chlorophyll biogenesis in embryo

2021 ◽  
Author(s):  
Chen Chen ◽  
Baixiao Niu ◽  
Zongju Yang ◽  
Tianqi Bai ◽  
Zhiguo E ◽  
...  
Keyword(s):  
Embryo Development ◽  
Chlorophyll Biosynthesis ◽  
Dual Role ◽  
Negative Regulator ◽  
Wild Type ◽  
Leaf Characteristics ◽  
Functional Conservation ◽  
True Leaf ◽  
Chlorophyll Biogenesis

Abstract The scutellum, coleoptile, coleorhiza, and epiblast (if it exists) consist of a complex embryonic envelope to protect the plumule and radicle inside a grass embryo. Controversies have been provoked for centuries regarding homologies of the grass embryonic structures. Here we found that the rice LEAFY COTYLEDONE1 (LEC1) gene, OsNF-YB7, is vital for embryo development. A leaf-like structure (LL) was developed from the scutellum of osnf-yb7 to replace the embryonic envelope that formed in wild-type. Additionally, osnf-yb7 developed chloroembryos due to overactivated chlorophyll biosynthesis. Thus, OsNF-YB7 likely plays a dual role in chlorophyll biogenesis in rice embryos: (1) OsNF-YB7 directly represses genes, such as rice GOLDED-LIKE1 (OsGLK1), involving chlorophyll biosynthesis; (2) OsNF-YB7 binds to OsGLK1 to repress the downstream genes of OsGLK1. Parallel phenotypes shown in osnf-yb7 and lec1 suggest functional conservation of the LEC1-type genes in plants. Both lec1 cotyledons and osnf-yb7 LL displayed true leaf characteristics. Our morphological and transcriptional evidence implied that LL replaces the embryonic envelope in osnf-yb7, raising the hypothesis that the grass embryonic envelope is an analog of Arabidopsis cotyledon. This study demonstrates that OsNF-YB7 acts as a negative regulator in chlorophyll biogenesis and is important for embryonic envelope formation.

scholarly journals Transcription Profile Analysis of Chlorophyll Biosynthesis in Leaves of Wild-Type and Chlorophyll b-Deficient Rice (Oryza sativa L.)

Agriculture ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 401
Author(s):  
Minh Khiem Nguyen ◽  
Tin-Han Shih ◽  
Szu-Hsien Lin ◽  
Jun-Wei Lin ◽  
Hoang Chinh Nguyen ◽  
...  
Keyword(s):  
Oryza Sativa ◽  
Core Protein ◽  
Profile Analysis ◽  
Oryza Sativa L ◽  
Electron Flow ◽  
Chlorophyll Biosynthesis ◽  
Wild Type ◽  
Transcription Analysis ◽  
Chl A ◽  
Chl Biosynthesis

Photosynthesis is an essential biological process and a key approach for raising crop yield. However, photosynthesis in rice is not fully investigated. This study reported the photosynthetic properties and transcriptomic profiles of chlorophyll (Chl) b-deficient mutant (ch11) and wild-type rice (Oryza sativa L.). Chl b-deficient rice revealed irregular chloroplast development (indistinct membranes, loss of starch granules, thinner grana, and numerous plastoglobuli). Next-generation sequencing approach application revealed that the differential expressed genes were related to photosynthesis machinery, Chl-biosynthesis, and degradation pathway in ch11. Two genes encoding PsbR (PSII core protein), FtsZ1, and PetH genes, were found to be down-regulated. The expression of the FtsZ1 and PetH genes resulted in disrupted chloroplast cell division and electron flow, respectively, consequently reducing Chl accumulation and the photosynthetic capacity of Chl b-deficient rice. Furthermore, this study found the up-regulated expression of the GluRS gene, whereas the POR gene was down-regulated in the Chl biosynthesis and degradation pathways. The results obtained from RT-qPCR analyses were generally consistent with those of transcription analysis, with the exception of the finding that MgCH genes were up-regulated which enhance the important intermediate products in the Mg branch of Chl biosynthesis. These results indicate a reduction in the accumulation of both Chl a and Chl b. This study suggested that a decline in Chl accumulation is caused by irregular chloroplast formation and down-regulation of POR genes; and Chl b might be degraded via the pheophorbide b pathway, which requires further elucidation.

RNF43 mutations to predict survival from treatment with immune checkpoint inhibitors and are associated with a high tumor mutation burden in bladder cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e16528-e16528
Author(s):  
Liping Li ◽  
Mengmei Yang ◽  
Mengli Huang
Keyword(s):  
Bladder Cancer ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Negative Regulator ◽  
Wilcoxon Test ◽  
Wild Type ◽  
Tumor Mutation Burden ◽  
Mutation Burden ◽  
The Impact

e16528 Background: Immune checkpoint inhibitors (ICIs) targeting PD-1/L1 have been approved as first-line treatment for cisplatin-ineligible patients and as second-line therapy for patients with metastatic urothelial carcinoma of the bladder. Biomarkers can help select patients who are more likely to response to ICIs. RNF43 is an E3 ubiquitin ligase that acts as a negative regulator of Wnt/β-catenin signaling pathway. In colorectal cancer (CRC) patients treated with immune checkpoint inhibitors (ICIs), RNF43 mutations predicted longer overall survival (OS). The impact of RNF43 mutations on the efficiency of ICIs in bladder cancer(BLC) remains to be explored. Methods: We downloaded the mutation and clinical data of 211 BLC patients treated with ICIs from the immunotherapeutic cohort published by Samstein et al. (2019). OS analyses were conducted using Kaplan-Meier curves and log-rank tests. Wilcoxon test was used for the comparison of TMB. We also downloaded a TCGA cohort for prognostic analysis. The correlations between RNF43 and immune infiltrates were analyzed in the TIMER2.0 database. Statistical significance was set at p = 0.05. Results: RNF43 mutations were identified in 4.3%(9/211) and 3%(13/438) BLC patients in the immunotherapeutic and TCGA cohort, respectively. In the immunotherapeutic cohort, patients with RNF43 mutations had significantly longer OS (25 months vs 8 months; p = 0.015) and higher tumor mutation burden(TMB, 42.3 vs 7.9; p = 3.15E-06) than RNF43-wild-type patients. Different from this, no significant difference was found in OS between RNF43-mutant and RNF43-wild-type BLC patients with standard treatment in the TCGA cohort (p = 0.696). These results indicated that RNF43 was not a prognostic factor but a predictive biomarker of survival in BLC treated with ICIs. No difference was observed in subsets of immune cells between RNF43-mutant and the RNF43-wide-type BLC patients, including neutrophils, macrophages, CD8+ T cells, Tregs, B cells and NK cells. Conclusions: RNF43 mutations may be a predictor of survival benefit from ICIs in bladder cancer and correlated with higher TMB. Further studies in other ICI-treated cohorts are needed to confirm these results.

scholarly journals Accumulation of Inorganic Polyphosphate in phoU Mutants of Escherichia coli and Synechocystis sp. Strain PCC6803

2002 ◽  
Vol 68 (8) ◽  
pp. 4107-4110 ◽  
Author(s):  
Tomohiro Morohoshi ◽  
Tatsuya Maruo ◽  
Yoko Shirai ◽  
Junichi Kato ◽  
Tsukasa Ikeda ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Type Strain ◽  
Wild Type Strain ◽  
Biological Process ◽  
Negative Regulator ◽  
Wild Type ◽  
Inorganic Polyphosphate ◽  
Insertional Inactivation ◽  
Synechocystis Sp ◽  
Polyp Accumulation

ABSTRACT The biological process for phosphate (Pi) removal is based on the use of bacteria capable of accumulating inorganic polyphosphate (polyP). We obtained Escherichia coli mutants which accumulate a large amount of polyP. The polyP accumulation in these mutants was ascribed to a mutation of the phoU gene that encodes a negative regulator of the Pi regulon. Insertional inactivation of the phoU gene also elevated the intracellular level of polyP in Synechocystis sp. strain PCC6803. The mutant could remove fourfold more Pi from the medium than the wild-type strain removed.

scholarly journals FK506-binding protein FklB is involved in biofilm formation through its peptidyl-prolyl isomerase activity

2020 ◽  
Author(s):  
Chrysoula Zografou ◽  
Maria Dimou ◽  
Panagiotis Katinakis
Keyword(s):  
Biofilm Formation ◽  
Negative Regulator ◽  
Cell Length ◽  
Wild Type ◽  
Prolyl Isomerase ◽  
Ppiase Activity ◽  
Peptidyl Prolyl Isomerase ◽  
Knock Out ◽  
E Coli ◽  
The Mean

AbstractFklB is a member of the FK506-binding proteins (FKBPs), a family that consists of five genes in Escherichia coli. Little is known about the physiological and functional role of FklB in bacterial movement. In the present study, FklB knock-out mutant ΔfklB presented an increased swarming and swimming motility and biofilm formation phenotype, suggesting that FklB is a negative regulator of these cellular processes. Complementation with Peptidyl-prolyl isomerase (PPIase)-deficient fklB gene (Y181A) revealed that the defects in biofilm formation were not restored by Y181A, indicating that PPIase activity of FklB is modulating biofilm formation in E. coli. The mean cell length of ΔfklB swarming cells was significantly smaller as compared to the wild-type BW25113. Furthermore, the mean cell length of swarming and swimming wild-type and ΔfklB cells overexpressing fklB or Y181A was considerably larger, suggesting that PPIase activity of FklB plays a role in cell elongation and/or cell division. A multi-copy suppression assay demonstrated that defects in motility and biofilm phenotype were compensated by overexpressing sets of PPIase-encoding genes. Taken together, our data represent the first report demonstrating the involvement of FklB in cellular functions of E. coli.

scholarly journals NITROGEN LIMITATION ADAPTATION functions as a negative regulator of Arabidopsis immunity

2021 ◽  
Author(s):  
Beatriz Val Torregrosa ◽  
Mireia Bundo ◽  
Tzyy Jen Chiou ◽  
Victor Flors ◽  
Blanca San Segundo
Keyword(s):  
Immune Responses ◽  
Transcriptional Activation ◽  
Fungal Pathogens ◽  
Nitrogen Limitation ◽  
Negative Regulator ◽  
Loss Of Function ◽  
Wild Type ◽  
Pathogen Infection ◽  
Fungal Elicitors ◽  
Resistance To Infection

Background: Phosphorus is an important macronutrient required for plant growth and development. It is absorbed through the roots in the form of inorganic phosphate (Pi). To cope with Pi limitation, plants have evolved an array of adaptive mechanisms to facilitate Pi acquisition and protect them from stress caused by Pi starvation. The NITROGEN LIMITATION ADAPTION (NLA) gene plays a key role in the regulation of phosphate starvation responses (PSR), its expression being regulated by the microRNA miR827. Stress caused by Pi limiting conditions might also affect the plant response to pathogen infection. However, cross-talk between phosphate signaling pathways and immune responses remains unclear. Results: In this study, we investigated whether NLA plays a role in Arabidopsis immunity. We show that loss-of-function of NLA and MIR827 overexpression causes an increase in phosphate (Pi) content which results in resistance to infection by the fungal pathogen Plectosphaerella cucumerina. The nla mutant plants accumulated callose in their leaves, a response that is also observed in wild-type plants that have been treated with high Pi. We also show that pathogen infection and treatment with fungal elicitors is accompanied by transcriptional activation of MIR827 and down-regulation of NLA. Upon pathogen challenge, nla plants exhibited higher levels of the phytoalexin camalexin compared to wild type plants. Camalexin level also increases in wild type plants treated with high Pi. Furthermore, the nla mutant plants accumulated salicylic acid (SA) and jasmonic acid (JA) in the absence of pathogen infection whose levels further increased upon pathogen. Conclusions: This study shows that NLA acts as a negative regulator of Arabidopsis immunity. Overaccumulation of Pi in nla plants positively affects resistance to infection by fungal pathogens. This piece of information reinforces the idea of signaling convergence between Pi and immune responses for the regulation of disease resistance in Arabidopsis.

scholarly journals Constitutive Photomorphogenic 1 Enhances ER Stress Tolerance in Arabidopsis

2021 ◽  
Vol 22 (19) ◽  
pp. 10772
Author(s):  
Chang Ho Kang ◽  
Eun Seon Lee ◽  
Ganesh M. Nawkar ◽  
Joung Hun Park ◽  
Seong Dong Wi ◽  
...  
Keyword(s):  
Stress Response ◽  
Er Stress ◽  
Stress Conditions ◽  
Negative Regulator ◽  
Light Signaling ◽  
Dependent Manner ◽  
Wild Type ◽  
Er Stress Response ◽  
The Unfolded Protein Response ◽  
Mutant Locus

Interaction between light signaling and stress response has been recently reported in plants. Here, we investigated the role of CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1), a key regulator of light signaling, in endoplasmic reticulum (ER) stress response in Arabidopsis. The cop1-4 mutant Arabidopsis plants were highly sensitive to ER stress induced by treatment with tunicarmycin (Tm). Interestingly, the abundance of nuclear-localized COP1 increased under ER stress conditions. Complementation of cop1-4 mutant plants with the wild-type or variant types of COP1 revealed that the nuclear localization and dimerization of COP1 are essential for its function in plant ER stress response. Moreover, the protein amount of ELONGATED HYPOCOTYL 5 (HY5), which inhibits bZIP28 to activate the unfolded protein response (UPR), decreased under ER stress conditions in a COP1-dependent manner. Accordingly, the binding of bZIP28 to the BIP3 promoter was reduced in cop1-4 plants and increased in hy5 plants compared with the wild type. Furthermore, introduction of the hy5 mutant locus into the cop1-4 mutant background rescued its ER stress-sensitive phenotype. Altogether, our results suggest that COP1, a negative regulator of light signaling, positively controls ER stress response by partially degrading HY5 in the nucleus.

scholarly journals Characterization of Plasmodium falciparum NEDD8 and identification of cullins as its substrates

2020 ◽  
Author(s):  
Manish Bhattacharjee ◽  
Navin Adhikari ◽  
Renu Sudhakar ◽  
Zeba Rizvi ◽  
Divya Das ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Plasmodium Falciparum ◽  
Western Blot ◽  
Wild Type ◽  
Malaria Parasites ◽  
Post Translational Modifications ◽  
Functional Conservation ◽  
Cellular Processes ◽  
Physiological Substrates

ABSTRACTA variety of post-translational modifications of Plasmodium falciparum proteins, including phosphorylation and ubiquitination, are shown to have key regulatory roles. The neural precursor cell expressed developmentally downregulated protein 8 (NEDD8) is a ubiquitin-like modifier of cullin-RING E3 ubiquitin ligases, which regulate diverse cellular processes, including the cell-cycle. Although neddylation pathway is conserved in eukaryotes, it is yet to be characterized in Plasmodium and related apicomplexan parasites. Towards studying the neddylation pathway in malaria parasites, we characterized P. falciparum NEDD8 (PfNEDD8) and identified cullins as its physiological substrates. PfNEDD8 is a 76 amino acid residue protein without the C-terminal tail, indicating that it can be readily conjugated. The wild type and mutant (Gly75Gly76 mutated to Ala75Ala76) PfNEDD8 were expressed in P. falciparum. Western blot of wild type PfNEDD8-expressing parasites indicated multiple high molecular weight conjugates, which were absent in the parasites expressing the mutant, indicating conjugation of NEDD8 to proteins through Gly76. Immunoprecipitation followed by mass spectrometry of wild type PfNEDD8-expressing parasites identified several proteins, including two putative cullins. Furthermore, we expressed PfNEDD8 in mutant S. cerevisiae strains that lacked endogenous NEDD8 (Δrub1) or NEDD8 conjugating E2 enzyme (ΔUbc12). The western blot of complemented strains and mass spectrometry of PfNEDD8 immunoprecipitate showed conjugation of PfNEDD8 to S. cerevisiae cullin cdc53, demonstrating functional conservation and cullins as the physiological substrates of PfNEDD8. The characterization of PfNEDD8 and identification of cullins as its substrates make ground for investigation of specific roles and drug target potential of neddylation pathway in malaria parasites.

scholarly journals Isolation and characterization of the SPT2 gene, a negative regulator of Ty-controlled yeast gene expression.

1985 ◽  
Vol 5 (7) ◽  
pp. 1543-1553 ◽  
Author(s):  
G S Roeder ◽  
C Beard ◽  
M Smith ◽  
S Keranen
Keyword(s):  
Gene Product ◽  
Regulatory Region ◽  
Negative Regulator ◽  
Transcriptional Level ◽  
Wild Type ◽  
Isolation And Characterization ◽  
Mutant Strains ◽  
Insertion Mutations ◽  
His4 Gene

The his4-917 mutation of Saccharomyces cerevisiae results from the insertion of the Ty element Ty917 into the regulatory region of the HIS4 gene and renders the cell His-. The hist4-912 delta mutant, which carries a solo delta in the 5'-noncoding region of HIS4, is His+ at 37 degrees C but His- at 23 degrees C. Both these mutations interfere with HIS4 expression at the transcriptional level. The His- phenotype of both insertion mutations is suppressed by mutations at the SPT2 locus. The product of the wild-type SPT2 gene apparently represses HIS4 transcription in these mutant strains; this repression is relieved when the SPT2 gene is destroyed by mutation. The repression of transcription by SPT2 presumably results from an interaction between the SPT2+ gene product and Ty or delta sequences. In this paper, we report the cloning and DNA sequence analysis of the wild-type SPT2 gene and show that the gene is capable of encoding a protein of 333 amino acids in length. In addition, we show that a dominant mutation of the SPT2 gene results from the generation of an ochre codon which is presumed to lead to a shortened SPT2 gene product.

Abstract 15445: The Sirtuin SIRT3 Blocks Doxorubicin-induced Cardiac Hypertrophic Response of Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Vinodkumar Pillai ◽  
Sadhana Samant ◽  
Nagalingam Sundaresan ◽  
Gene Kim ◽  
Mahesh P Gupta
Keyword(s):  
Negative Regulator ◽  
Neonatal Rat ◽  
Whole Body ◽  
Wild Type ◽  
Electron Microscopic ◽  
Specific Expression ◽  
Rat Cardiomyocytes ◽  
Fluorescent Intensity ◽  
Hypertrophic Response

Background and objective: Doxorubicin is a chemotherapeutic drug widely used to treat variety of cancers. One of the serious side effects of doxorubicin is its toxicity to the heart. Previously, we have shown that overexpression of SIRT3 blocks the hypertrophic response of the heart to agonist treatments. This study was undertaken to investigate whether SIRT3 can also attenuate the doxorubicin-induced cardiac hypertrophic response in mice. Methods and results: Neonatal rat cardiomyocytes overexpressed with SIRT3 and treated with doxorubicin (10μM) showed 28% reduced mean fluorescent intensity for CM-H 2 DCFDA dye, compared to mock infected control cells treated with doxorubicin, thus suggesting that SIRT3 was capable of blocking doxorubicin-induced ROS synthesis in cardiomyocytes. To examine the cardioprotective effects of SIRT3 in doxorubicin-induced cardiotoxicity in vivo ; we used a cumulative dose of 15mg/kg of doxorubicin for two different time points. One group of mice was treated intraperitoneally with 5mg/kg doxorubicin or an equal volume of saline every two weeks for a total of three doses. Transgenic mice having cardiac specific expression of SIRT3 (SIRT3-Tg) showed 33% reduced HW/BW ratio compared to control mice. Echocardiographic evaluation of hearts showed significantly reduced fractional shortening in control mice, compared to SIRT3-Tg mice (24.6 vs 34.7 %, P<0.05). SIRT3-Tg mice also showed significantly reduced fetal gene expression for ANF, βMHC and collagen-1 as determined by RT-PCR. Masson’s trichrome staining showed significantly reduced fibrosis in doxorubicin treated SIRT3-Tg mice compared to its control. Furthermore, electron microscopic analysis showed preserved mitochondrial and sarcomeres structures in doxorubicin treated SIRT3-Tg hearts, whereas in wild-type hearts these structures were highly disorganized. Second group of mice that received 15mg/kg dose for two weeks also showed similar results. Contrary to this, whole body SIRT3 knockout mice showed exacerbated cardiac hypertrophic response compared to wild-type mice in response to doxorubicin treatment. Conclusion: These results demonstrated that SIRT3 is an endogenous negative regulator of doxorubicin-induced cardiac hypertrophic response.

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