scholarly journals Comparative RNA-Seq Analysis Reveals That Regulatory Network of Maize Root Development Controls the Expression of Genes in Response to N Stress

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0151697 ◽  
Author(s):  
Xiujing He ◽  
Haixia Ma ◽  
Xiongwei Zhao ◽  
Shujun Nie ◽  
Yuhua Li ◽  
...  
Author(s):  
Laura Ravazzolo ◽  
Stéphanie Boutet-Mercey ◽  
François Perreau ◽  
Cristian Forestan ◽  
Serena Varotto ◽  
...  

Abstract In maize, nitrate regulates root development thanks to the coordinated action of many players. In this study, the involvement of SLs and auxin as putative components of the nitrate regulation of lateral root was investigated. To this aim, the endogenous SL content of maize root in response to nitrate was assessed by LC-MS/MS and measurements of lateral root density in the presence of analogues or inhibitors of auxin and strigolactones were performed. Furthermore, an untargeted RNA-seq based approach was used to better characterize the participation of auxin and strigolactones to the transcriptional signature of maize root response to nitrate. Our results suggested that N deprivation induces zealactone and carlactonoic acid biosynthesis in root, to a higher extent if compared to P-deprived roots. Moreover, data on lateral root density led to hypothesise that the induction of LR development early occurring upon nitrate supply involves the inhibition of SL biosynthesis, but that the downstream target of SL shutdown, beside auxin, includes also additional unknown players. Furthermore, RNA-seq results provided a set of putative markers for the auxin- or SL-dependent action of nitrate, meanwhile allowing to identify also novel components of the molecular regulation of maize root response to nitrate. Globally the existence of at least four different pathways was hypothesised, one dependent on auxin, a second one mediated by SLs, a third deriving from the SL-auxin interplay and one last attributable to nitrate itself through further downstream signals. Further work will be necessary to better assess the reliability of the model proposed.


BMC Genomics ◽  
2014 ◽  
Vol 15 (1) ◽  
pp. 230 ◽  
Author(s):  
David Secco ◽  
Huixia Shou ◽  
James Whelan ◽  
Oliver Berkowitz

2021 ◽  
Vol 22 (11) ◽  
pp. 5902
Author(s):  
Stefan Nagel ◽  
Claudia Pommerenke ◽  
Corinna Meyer ◽  
Hans G. Drexler

Recently, we documented a hematopoietic NKL-code mapping physiological expression patterns of NKL homeobox genes in human myelopoiesis including monocytes and their derived dendritic cells (DCs). Here, we enlarge this map to include normal NKL homeobox gene expressions in progenitor-derived DCs. Analysis of public gene expression profiling and RNA-seq datasets containing plasmacytoid and conventional dendritic cells (pDC and cDC) demonstrated HHEX activity in both entities while cDCs additionally expressed VENTX. The consequent aim of our study was to examine regulation and function of VENTX in DCs. We compared profiling data of VENTX-positive cDC and monocytes with VENTX-negative pDC and common myeloid progenitor entities and revealed several differentially expressed genes encoding transcription factors and pathway components, representing potential VENTX regulators. Screening of RNA-seq data for 100 leukemia/lymphoma cell lines identified prominent VENTX expression in an acute myelomonocytic leukemia cell line, MUTZ-3 containing inv(3)(q21q26) and t(12;22)(p13;q11) and representing a model for DC differentiation studies. Furthermore, extended gene analyses indicated that MUTZ-3 is associated with the subtype cDC2. In addition to analysis of public chromatin immune-precipitation data, subsequent knockdown experiments and modulations of signaling pathways in MUTZ-3 and control cell lines confirmed identified candidate transcription factors CEBPB, ETV6, EVI1, GATA2, IRF2, MN1, SPIB, and SPI1 and the CSF-, NOTCH-, and TNFa-pathways as VENTX regulators. Live-cell imaging analyses of MUTZ-3 cells treated for VENTX knockdown excluded impacts on apoptosis or induced alteration of differentiation-associated cell morphology. In contrast, target gene analysis performed by expression profiling of knockdown-treated MUTZ-3 cells revealed VENTX-mediated activation of several cDC-specific genes including CSFR1, EGR2, and MIR10A and inhibition of pDC-specific genes like RUNX2. Taken together, we added NKL homeobox gene activities for progenitor-derived DCs to the NKL-code, showing that VENTX is expressed in cDCs but not in pDCs and forms part of a cDC-specific gene regulatory network operating in DC differentiation and function.


Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 630
Author(s):  
Yongqing Lan ◽  
Meng Li ◽  
Shuangli Mi

Hematopoietic differentiation is a well-orchestrated process by many regulators such as transcription factor and long non-coding RNAs (lncRNAs). However, due to the large number of lncRNAs and the difficulty in determining their roles, the study of lncRNAs is a considerable challenge in hematopoietic differentiation. Here, through gene co-expression network analysis over RNA-seq data generated from representative types of mouse myeloid cells, we obtained a catalog of potential key lncRNAs in the context of mouse myeloid differentiation. Then, employing a widely used in vitro cell model, we screened a novel lncRNA, named Gdal1 (Granulocytic differentiation associated lncRNA 1), from this list and demonstrated that Gdal1 was required for granulocytic differentiation. Furthermore, knockdown of Cebpe, a principal transcription factor of granulocytic differentiation regulation, led to down-regulation of Gdal1, but not vice versa. In addition, expression of genes involved in myeloid differentiation and its regulation, such as Cebpa, were influenced in Gdal1 knockdown cells with differentiation blockage. We thus systematically identified myeloid differentiation associated lncRNAs and substantiated the identification by investigation of one of these lncRNAs on cellular phenotype and gene regulation levels. This study promotes our understanding of the regulation of myeloid differentiation and the characterization of roles of lncRNAs in hematopoietic system.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Matthew Stratton ◽  
Ashley Francois ◽  
Oscar Bermeo-Blanco ◽  
Alessandro Canella ◽  
Lynn Marcho ◽  
...  

Over 6 million Americans suffer from heart failure (HF) while the 5-year mortality rate following first admission for HF is over 40%. Cardiac fibrosis is a clinical hallmark of HF, regardless of the initiating pathology and is thought to contribute to disease progression. Using an epigenomics discovery approach, we uncovered a nuclear protein, Sertad4, as a potential anti-fibrotic target. Our data indicate that Sertad4 is a positive regulator of fibroblast activation. Specifically, cultured cardiac fibroblast experiments demonstrate that Sertad4 targeting with shRNAs blocks fibroblast proliferation and causes cells to arrest in the G2/M phase of the cell cycle. Also, shRNA targeting of Sertad4 dramatically blocked activation of myofibroblast differentiation genes (αSMA/POSTN/COL1A1). Mechanistically, these effects appear to be mediated by Sertad4 regulation of SMAD2 protein stability in the presence of TGF-β1 stimulation as demonstrated by proteasome inhibition experiments. RNA-seq analysis indicate that Sertad4 also regulates the expression of genes involved in ubiquitination and proteasome degradation. Next, we sought to determine the effect of global Sertad4 knockout on post-myocardial infarct (MI) remodeling and cardiac function in mice. After 4 weeks of permanent LAD ligation, echocardiography was performed to measure systolic function. Relative to wild-type (WT) controls, the Sertad4 KO mice showed preserved systolic function as evident by improved ejection fraction (WT 14.4 +/- 3.6 vs. KO 33.9+/-5.9, p=0.035) and fractional shortening (WT 6.5 +/- 1.7 vs. KO 16.4 +/- 3.4, p=0.046). β-gal staining in the Sertad4/LacZ reporter mouse subjected to MI showed robust Sertad4/LacZ expression in the ischemic scar and boarder-zone with almost no expression in control hearts. This data supports the notion that Sertad4 has a key role in cardiac remodeling in response to ischemic injury.


2021 ◽  
Author(s):  
Jing Wang ◽  
Tianjie Chen ◽  
Xiaohua Zhang ◽  
Shulei Zhao

Abstract Long noncoding RNAs (lncRNAs) play important roles in the occurrence and development of many diseases and can be used as targets for diagnosis and treatment. However, the expression and function of lncRNAs in the injury and repair of acute pancreatitis (AP) are unclear. To decipher lncRNAs’ regulatory roles in AP, we reanalyzed an RNA-seq dataset of 24 pancreatic tissues, including those of normal control mice (BL), those 7 days after mild AP (D7), and those 14 days after mild AP (D14). The results showed significant differences in lncRNA and mRNA expression of D7/D14 groups compared with the control group. Co-expression analysis showed that differentially expressed (DE) lncRNAs were closely related to immunity- and inflammation-related pathways by trans-regulating mRNA expression. The lncRNA–mRNA network showed that the lncRNAs Dancer, Gmm20488, Terc, Snhg3, and Snhg20 were significantly correlated with AP pathogenesis. WGCNA and cis regulation analysis also showed that AP repair-associated lncRNAs were correlated with extracellular and inflammation-related genes, which affect the repair and regeneration of pancreatic injury after AP. In conclusion, the systemic dysregulation of lncRNAs is strongly involved in remodeling AP’s gene expression regulatory network, and the lncRNA–mRNA expression network could identify targets for AP treatment and damage repair.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 2748 ◽  
Author(s):  
Andrea Komljenovic ◽  
Julien Roux ◽  
Marc Robinson-Rechavi ◽  
Frederic B. Bastian

BgeeDB is a collection of functions to import into R re-annotated, quality-controlled and reprocessed expression data available in the Bgee database. This includes data from thousands of wild-type healthy samples of multiple animal species, generated with different gene expression technologies (RNA-seq, Affymetrix microarrays, expressed sequence tags, and in situ hybridizations). BgeeDB facilitates downstream analyses, such as gene expression analyses with other Bioconductor packages. Moreover, BgeeDB includes a new gene set enrichment test for preferred localization of expression of genes in anatomical structures (“TopAnat”). Along with the classical Gene Ontology enrichment test, this test provides a complementary way to interpret gene lists. Availability: http://www.bioconductor.org/packages/BgeeDB/


2019 ◽  
Vol 15 (11) ◽  
pp. e1007435 ◽  
Author(s):  
Jiajun Zhang ◽  
Wenbo Zhu ◽  
Qianliang Wang ◽  
Jiayu Gu ◽  
L. Frank Huang ◽  
...  

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