scholarly journals The SlHB8 Acts as a Negative Regulator in Stem Development and Lignin Biosynthesis

2021 ◽  
Vol 22 (24) ◽  
pp. 13343
Author(s):  
Xiaojuan Liu ◽  
Caiyu Wu ◽  
Deding Su ◽  
Yang Yang ◽  
Zhiqiang Xian ◽  
...  
Keyword(s):  
Leucine Zipper ◽  
Expression Profiles ◽  
Lignin Biosynthesis ◽  
Stem Diameter ◽  
Negative Regulator ◽  
Biosynthesis Pathway ◽  
Loss Of Function ◽  
Class Iii ◽  
Cell Layers ◽  
Stem Development

The stem is an important organ in supporting plant body, transporting nutrients and communicating signals for plant growing. However, studies on the regulation of stem development in tomato are rather limited. In our study, we demonstrated that SlHB8 negatively regulated tomato stem development. SlHB8 belongs to homeo domain-leucine zipper Class III gene family transcription factors and expressed in all the organs examined including root, stem, leaves, flower, and fruit. Among these tissues, SlHB8 showed stable high expression level during tomato stem development. Overexpression of SlHB8 gene decreased stem diameter with inhibited xylem width and xylem cell layers, while loss of function of SlHB8gene increased the stem diameter and xylem width. The contents of lignin were decreased both in leaves and stems of SlHB8 overexpression plants. RNA-seq analysis on the stems of wild type and SlHB8 transgenic plants showed that the 116 DEGs (differential expressed genes) with reversible expression profiles in SlHB8-ox and SlHB8-cr plants were significantly enriched in the phenylpropanoid biosynthesis pathway and plant-pathogen pathway which were related to lignin biosynthesis and disease resistance. Meanwhile, the key genes involved in the lignin biosynthesis pathway such as SlCCR (cinnamoyl-CoA reductase), SlCYP73A14/C4H (cinnamate 4-hydroxylase), SlC3H (coumarate 3-hydroxylase) and SlCAD (cinnamoyl alcohol dehydrogenase) were down-regulated in both stem and leaves of SlHB8 overexpression plants, indicating a negative regulatory role of SlHB8 in the lignin biosynthesis and stem development.

scholarly journals GENE-34. THERAPEUTICALLY TARGETING EPIGENOMIC AND TRANSCRIPTIONAL DYSFUNCTION IN ATRX-DEFICIENT GLIOMA

2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi104-vi105 ◽  
Author(s):  
Carla Danussi ◽  
Anand Singh ◽  
Pavan Pinnamaneni ◽  
Grant Fisher ◽  
David Picketts ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Hdac Inhibitors ◽  
Cellular Motility ◽  
Loss Of Function ◽  
Class Iii ◽  
Lineage Specification ◽  
Specific Chemical ◽  
Molecular Alterations ◽  
Genome Wide ◽  
Astrocytic Differentiation

Abstract Diffusely infiltrating gliomas feature loss-of-function mutations in the chromatin remodeler gene ATRX as defining molecular alterations delineating major adult and pediatric disease subtypes. We recently reported that Atrx deficiency drives glioma-relevant phenotypes, such as increased motility and astrocytic differentiation profiles, by directly modulating epigenomic landscapes and the corresponding transcriptional profiles in glioma cells of origin. In particular, Atrx deficiency was associated with disruptions in H3.3 histone content at key genetic loci. To further understand the downstream epigenomic dysfunction induced by ATRX deficiency, we compared genome-wide chromatin-state maps of Atrx+ and Atrx- primary murine neuroepithelial progenitors (mNPCs). This ChIP–seq analysis revealed major differences in the localization of heterochromatin repressive marks H3K9me3 and H3K27me3. Specifically, we identified peculiar locations in the genome displaying H3K9me3 depletion and gain of H3K27me3 upon Atrx inactivation. Interestingly, these regions were flanked by Atrx binding sites and perfectly co-localized with Lamina-Associated Domains, known to play important roles in tissue lineage specification. To better target this dysfunction, we utilized the Broad Institute Connectivity Map (CLUE analysis) to identify compounds likely to revert the unique transcriptional perturbations induced by Atrx deficiency. We found that HDAC inhibitors, as a compound class, yielded expression profiles strongly anticorrelated to those driven by Atrx deficiency in these datasets. Further integrating existing gene expression data from our mNPCs and the TCGA LGG project with our CLUE findings highlighted SIRT2, a class III HDAC, as a top potential target. SIRT2 expression was significantly upregulated in both Atrx- mNPCs and in ATRX-mutant gliomas and its specific chemical inhibition normalized cellular motility in both Atrx- mNPCs and ATRX-mutant, patient derived glioma stem cells. These findings indicate that SIRT2 inhibition represents a viable strategy to revert the epigenetic effects of ATRX deficiency on facultative heterochromatin and their transcriptional and phenotypic consequences.

scholarly journals Comparative RNA-Sequence Transcriptome Analysis of Phenolic Acid Metabolism in Salvia miltiorrhiza, a Traditional Chinese Medicine Model Plant

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Zhenqiao Song ◽  
Linlin Guo ◽  
Tian Liu ◽  
Caicai Lin ◽  
Jianhua Wang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Phenolic Acid ◽  
Expression Profiles ◽  
Salvia Miltiorrhiza ◽  
Lignin Biosynthesis ◽  
Biosynthesis Pathway ◽  
Acid Biosynthesis ◽  
The Core ◽  
Phenylpropanoid Biosynthesis

Salvia miltiorrhiza Bunge is an important traditional Chinese medicine (TCM). In this study, two S. miltiorrhiza genotypes (BH18 and ZH23) with different phenolic acid concentrations were used for de novo RNA sequencing (RNA-seq). A total of 170,787 transcripts and 56,216 unigenes were obtained. There were 670 differentially expressed genes (DEGs) identified between BH18 and ZH23, 250 of which were upregulated in ZH23, with genes involved in the phenylpropanoid biosynthesis pathway being the most upregulated genes. Nine genes involved in the lignin biosynthesis pathway were upregulated in BH18 and thus result in higher lignin content in BH18. However, expression profiles of most genes involved in the core common upstream phenylpropanoid biosynthesis pathway were higher in ZH23 than that in BH18. These results indicated that genes involved in the core common upstream phenylpropanoid biosynthesis pathway might play an important role in downstream secondary metabolism and demonstrated that lignin biosynthesis was a putative partially competing pathway with phenolic acid biosynthesis. The results of this study expanded our understanding of the regulation of phenolic acid biosynthesis in S. miltiorrhiza.

scholarly journals The Cotton Lignin Biosynthetic Gene Gh4CL30 Regulates Lignification and Phenolic Content and Contributes to Verticillium Wilt Resistance

2021 ◽  
pp. MPMI-03-20-0071
Author(s):  
Xian-Peng Xiong ◽  
Shi-Chao Sun ◽  
Qian-Hao Zhu ◽  
Xin-Yu Zhang ◽  
Yan-Jun Li ◽  
...  
Keyword(s):  
Verticillium Wilt ◽  
Expression Profiles ◽  
Lignin Biosynthesis ◽  
Biosynthesis Pathway ◽  
Virus Induced Gene Silencing ◽  
Cotton Production ◽  
Hub Genes ◽  
Time Points ◽  
Before And After ◽  
Open Access Article

Verticillium wilt is a vascular disease causing tremendous damage to cotton production worldwide. However, our knowledge of the mechanisms of cotton resistance or susceptibility to this disease is very limited. In this study, we compared the defense transcriptomes of cotton (Gossypium hirsutum) cultivars Shidalukang 1 (Verticillium dahliae resistant, HR) and Junmian 1 (V. dahliae susceptible, HS) before and after V. dahliae infection, identified hub genes of the network associated with responses to V. dahliae infection, and functionally characterized one of the hub genes involved in biosynthesis of lignin and phenolics. We identified 6,831 differentially expressed genes (DEGs) between the basal transcriptomes of HR and HS; 3,685 and 3,239 of these DEGs were induced in HR and HS, respectively, at different time points after V. dahliae infection. KEGG pathway analysis indicated that DEGs were enriched for genes involved in lignin biosynthesis. In all, 23 hub genes were identified based on a weighted gene coexpression network analysis of the 6,831 DEGs and their expression profiles at different time points after V. dahliae infection. Knockdown of Gh4CL30, one of the hub genes related to the lignin biosynthesis pathway, by virus-induced gene silencing, led to a decreased content of flavonoids, lignin, and S monomer but an increased content of G monomer, G/S lignin monomer, caffeic acid, and ferulic acid, and enhanced cotton resistance to V. dahliae. These results suggest that Gh4CL30 is a key gene modulating the outputs of different branches of the lignin biosynthesis pathway, and provide new insights into cotton resistance to V. dahliae. [Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

scholarly journals Control of stem cell niche and fruit development in Arabidopsis thaliana by AGO10/ZWL requires the bHLH transcription factor INDEHISCENT

2020 ◽  
Author(s):  
Manoj Valluru ◽  
Karim Sorefan
Keyword(s):  
Transcription Factor ◽  
Embryonic Development ◽  
Pluripotent Stem Cells ◽  
Apical Meristem ◽  
Leucine Zipper ◽  
Bhlh Transcription Factor ◽  
Loss Of Function ◽  
Class Iii ◽  
Auxin Transporter ◽  
Cell Niche

AbstractBackgroundThe shoot apical meristem (SAM) in plants is composed of a small mound of pluripotent stem cells that generate new organs. ARGONAUTE10 (AGO10) is known to be critical for maintenance of the embryonic SAM by regulating the expression of Class III HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP III) transcription factors, which then modulate downstream responses to the key phytohormone auxin. However, we do not understand how AGO10 modulates auxin responses after embryogenesis in the mature plant.ResultsHere we show that AGO10 regulates auxin responses in the post-embryonic SAM via the bHLH transcription factor INDEHISCENT (IND). IND directly regulates auxin responses in the SAM regulating the auxin transporter PIN1 via direct transcriptional regulation of PINOID kinase. We show that a loss of function ind mutation significantly restores ago10zwl-3 mutant SAM and fruit phenotypes. ago10zwl-3 mutants overexpress IND and overexpression of IND phenocopies the ago10zwl-3 SAM phenotypes, and regulates auxin transport and responses in the SAM. AGO10 also regulates post-embryonic development in the fruit via a similar genetic pathway.ConclusionsWe characterise a molecular mechanism that is conserved during post embryonic development linking AGO10 directly to auxin responses.

scholarly journals Insight into the bZIP Gene Family in Solanum tuberosum: Genome and Transcriptome Analysis to Understand the Roles of Gene Diversification in Spatiotemporal Gene Expression and Function

2020 ◽  
Vol 22 (1) ◽  
pp. 253
Author(s):  
Venura Herath ◽  
Jeanmarie Verchot
Keyword(s):  
Gene Expression ◽  
Gene Family ◽  
Functional Groups ◽  
Leucine Zipper ◽  
Expression Profiles ◽  
Crop Improvement ◽  
Potato Virus X ◽  
Tissue Growth ◽  
Abiotic Stress Response ◽  
Sequence Alignments

The basic region-leucine zipper (bZIP) transcription factors (TFs) form homodimers and heterodimers via the coil–coil region. The bZIP dimerization network influences gene expression across plant development and in response to a range of environmental stresses. The recent release of the most comprehensive potato reference genome was used to identify 80 StbZIP genes and to characterize their gene structure, phylogenetic relationships, and gene expression profiles. The StbZIP genes have undergone 22 segmental and one tandem duplication events. Ka/Ks analysis suggested that most duplications experienced purifying selection. Amino acid sequence alignments and phylogenetic comparisons made with the Arabidopsis bZIP family were used to assign the StbZIP genes to functional groups based on the Arabidopsis orthologs. The patterns of introns and exons were conserved within the assigned functional groups which are supportive of the phylogeny and evidence of a common progenitor. Inspection of the leucine repeat heptads within the bZIP domains identified a pattern of attractive pairs favoring homodimerization, and repulsive pairs favoring heterodimerization. These patterns of attractive and repulsive heptads were similar within each functional group for Arabidopsis and S. tuberosum orthologs. High-throughput RNA-seq data indicated the most highly expressed and repressed genes that might play significant roles in tissue growth and development, abiotic stress response, and response to pathogens including Potato virus X. These data provide useful information for further functional analysis of the StbZIP gene family and their potential applications in crop improvement.

scholarly journals Keap1 deletion accelerates mutant K-ras/p53-driven cholangiocarcinoma

2020 ◽  
Vol 318 (3) ◽  
pp. G419-G427 ◽  
Author(s):  
Tatsuhide Nabeshima ◽  
Shin Hamada ◽  
Keiko Taguchi ◽  
Yu Tanaka ◽  
Ryotaro Matsumoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cancer Progression ◽  
Stress Responses ◽  
Target Genes ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Related Factor ◽  
Loss Of Function ◽  
P53 Expression ◽  
Nrf2 Activation

The activation of the Kelch-like ECH-associated protein 1 (Keap1)-NF-E2-related factor 2 (Nrf2) pathway contributes to cancer progression in addition to oxidative stress responses. Loss-of-function Keap1 mutations were reported to activate Nrf2, leading to cancer progression. We examined the effects of Keap1 deletion in a cholangiocarcinoma mouse model using a mutant K-ras/ p53 mouse. Introduction of the Keap1 deletion into liver-specific mutant K-ras/ p53 expression resulted in the formation of invasive cholangiocarcinoma. Comprehensive analyses of the gene expression profiles identified broad upregulation of Nrf2-target genes such as Nqo1 and Gstm1 in the Keap1-deleted mutant K-ras/ p53 expressing livers, accompanied by upregulation of cholangiocyte-related genes. Among these genes, the transcriptional factor Sox9 was highly expressed in the dysplastic bile duct. The Keap-Nrf2-Sox9 axis might serve as a novel therapeutic target for cholangiocarcinoma. NEW & NOTEWORTHY The Keap1-Nrf2 system has a wide variety of effects in addition to the oxidative stress response in cancer cells. Addition of the liver-specific Keap1 deletion to mice harboring mutant K-ras and p53 accelerated cholangiocarcinoma formation, together with the hallmarks of Nrf2 activation. This process involved the expansion of Sox9-positive cells, indicating increased differentiation toward the cholangiocyte phenotype.

scholarly journals Genetic and Molecular Characterization of the Caenorhabditis elegans Gene, mel-26, a Postmeiotic Negative Regulator of MEI-1, a Meiotic-Specific Spindle Component

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 119-128
Author(s):  
M Rhys Dow ◽  
Paul E Mains
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Interactions ◽  
Negative Regulator ◽  
Meiotic Spindle ◽  
Loss Of Function ◽  
Protein Protein Interactions ◽  
Gain Of Function ◽  
Recessive Mutations ◽  
Female Germline

Abstract We have previously described the gene mei-1, which encodes an essential component of the Caenorhabditis elegans meiotic spindle. When ectopically expressed after the completion of meiosis, mei-1 protein disrupts the function of the mitotic cleavage spindles. In this article, we describe the cloning and the further genetic characterization of mel-26, a postmeiotic negative regulator of mei-1. mel-26 was originally identified by a gain-of-function mutation. We have reverted this mutation to a loss-of-function allele, which has recessive phenotypes identical to the dominant defects of its gain-of-function parent. Both the dominant and recessive mutations of mel-26 result in mei-1 protein ectopically localized in mitotic spindles and centrosomes, leading to small and misoriented cleavage spindles. The loss-of-function mutation was used to clone mel-26 by transformation rescue. As suggested by genetic results indicating that mel-26 is required only maternally, mel-26 mRNA was expressed predominantly in the female germline. The gene encodes a protein that includes the BTB motif, which is thought to play a role in protein-protein interactions.

scholarly journals Targeting hydroxycinnamoyl CoA: shikimate hydroxycinnamoyl transferase for lignin modification in Brachypodium distachyon

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Juan Carlos Serrani-Yarce ◽  
Luis Escamilla-Trevino ◽  
Jaime Barros ◽  
Lina Gallego-Giraldo ◽  
Yunqiao Pu ◽  
...  
Keyword(s):  
Negative Impact ◽  
Lignin Content ◽  
Brachypodium Distachyon ◽  
Lignin Biosynthesis ◽  
Reverse Direction ◽  
Wall Structure ◽  
Kinetic Properties ◽  
Loss Of Function ◽  
Down Regulation ◽  
Lignin Modification

Abstract Background Hydroxycinnamoyl CoA: shikimate hydroxycinnamoyl transferase (HCT) is a central enzyme of the so-called “esters” pathway to monolignols. As originally envisioned, HCT functions twice in this pathway, to form coumaroyl shikimate and then, in the “reverse” direction, to convert caffeoyl shikimate to caffeoyl CoA. The discovery of a caffeoyl shikimate esterase (CSE) that forms caffeic acid directly from caffeoyl shikimate calls into question the need for the reverse HCT reaction in lignin biosynthesis. Loss of function of HCT gives severe growth phenotypes in several dicot plants, but less so in some monocots, questioning whether this enzyme, and therefore the shikimate shunt, plays the same role in both monocots and dicots. The model grass Brachypodium distachyon has two HCT genes, but lacks a classical CSE gene. This study was therefore conducted to evaluate the utility of HCT as a target for lignin modification in a species with an “incomplete” shikimate shunt. Results The kinetic properties of recombinant B. distachyon HCTs were compared with those from Arabidopsis thaliana, Medicago truncatula, and Panicum virgatum (switchgrass) for both the forward and reverse reactions. Along with two M. truncatula HCTs, B. distachyon HCT2 had the least kinetically unfavorable reverse HCT reaction, and this enzyme is induced when HCT1 is down-regulated. Down regulation of B. distachyon HCT1, or co-down-regulation of HCT1 and HCT2, by RNA interference led to reduced lignin levels, with only modest changes in lignin composition and molecular weight. Conclusions Down-regulation of HCT1, or co-down-regulation of both HCT genes, in B. distachyon results in less extensive changes in lignin content/composition and cell wall structure than observed following HCT down-regulation in dicots, with little negative impact on biomass yield. Nevertheless, HCT down-regulation leads to significant improvements in biomass saccharification efficiency, making this gene a preferred target for biotechnological improvement of grasses for bioprocessing.

Hes1 is a negative regulator of inner ear hair cell differentiation

Development ◽  
2000 ◽  
Vol 127 (21) ◽  
pp. 4551-4560 ◽  
Author(s):  
J.L. Zheng ◽  
J. Shou ◽  
F. Guillemot ◽  
R. Kageyama ◽  
W.Q. Gao
Keyword(s):  
Cell Differentiation ◽  
Hair Cell ◽  
Inner Ear ◽  
Cell Fate ◽  
Hair Cells ◽  
Outer Hair Cells ◽  
Negative Regulator ◽  
Pcr Analysis ◽  
Loss Of Function ◽  
Hair Cell Differentiation

Hair cell fate determination in the inner ear has been shown to be controlled by specific genes. Recent loss-of-function and gain-of-function experiments have demonstrated that Math1, a mouse homolog of the Drosophila gene atonal, is essential for the production of hair cells. To identify genes that may interact with Math1 and inhibit hair cell differentiation, we have focused on Hes1, a mammalian hairy and enhancer of split homolog, which is a negative regulator of neurogenesis. We report here that targeted deletion of Hes1 leads to formation of supernumerary hair cells in the cochlea and utricle of the inner ear. RT-PCR analysis shows that Hes1 is expressed in inner ear during hair cell differentiation and its expression is maintained in adulthood. In situ hybridization with late embryonic inner ear tissue reveals that Hes1 is expressed in supporting cells, but not hair cells, of the vestibular sensory epithelium. In the cochlea, Hes1 is selectively expressed in the greater epithelial ridge and lesser epithelial ridge regions which are adjacent to inner and outer hair cells. Co-transfection experiments in postnatal rat explant cultures show that overexpression of Hes1 prevents hair cell differentiation induced by Math1. Therefore Hes1 can negatively regulate hair cell differentiation by antagonizing Math1. These results suggest that a balance between Math1 and negative regulators such as Hes1 is crucial for the production of an appropriate number of inner ear hair cells.

Sign in / Sign up

Export Citation Format

Share Document