scholarly journals The receptor-like cytoplasmic kinase MAZZA and CLAVATA-family receptors interact in vivo, together mediating developmental processes in Arabidopsis thaliana

2020 ◽  
Author(s):  
Patrick Blümke ◽  
Jenia Schlegel ◽  
Sabine Becher ◽  
Karine Pinto ◽  
Rüdiger Simon
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Plasma Membrane ◽  
Root Development ◽  
Target Gene ◽  
Size Control ◽  
Receptor Complexes ◽  
Cle Peptide ◽  
Developmental Contexts

AbstractThe receptor-like kinases (RLKs) CLAVATA1 (CLV1) and BARELY ANY MERISTEMs (BAM1 – 3) form the CLV-family (CLVf), which perceives peptides of the CLV3/EMBRYO SURROUNDING REGION (ESR)-related (CLE) family within various signaling pathways of Arabidopsis thaliana. CLE peptide signaling, which is required for meristem size control, vascular development, or pathogen responses, involves the formation of receptor complexes at the plasma membrane (PM). These complexes comprise RLKs and co-receptors in varying compositions depending on the signaling context and regulate target gene expression, such as WUSCHEL (WUS). How the CLE signal is transmitted intracellularly after perception at the PM is not known.Here, we found that the membrane-associated receptor-like cytoplasmic kinase (RLCK) MAZZA (MAZ) MAZ and additional members of the Pti1-like protein family interact in vivo with CLVf receptors. MAZ, which is widely expressed throughout the plant, localizes to the PM via posttranslational palmitoylation potentially enabling stimulus-triggered protein re-localization. We identified a role for a CLV1/MAZ signaling module during stomatal and root development, and redundancy could potentially mask other phenotypes of maz-1 mutants. We propose that RLCKs such as MAZ mediate CLVf signaling in a variety of developmental contexts, paving the way towards understanding the intracellular processes after CLE peptide perception.

Mutants of cubitus interruptus that are independent of PKA regulation are independent of hedgehog signaling

Development ◽  
1999 ◽  
Vol 126 (16) ◽  
pp. 3607-3616 ◽  
Author(s):  
Y. Chen ◽  
J.R. Cardinaux ◽  
R.H. Goodman ◽  
S.M. Smolik
Keyword(s):  
Gene Expression ◽  
Target Gene ◽  
Ectopic Expression ◽  
Proteolytic Processing ◽  
Dominant Negative ◽  
Cubitus Interruptus ◽  
Target Gene Expression ◽  
Exogenous Expression

Hedgehog (HH) is an important morphogen involved in pattern formation during Drosophila embryogenesis and disc development. cubitus interruptus (ci) encodes a transcription factor responsible for transducing the hh signal in the nucleus and activating hh target gene expression. Previous studies have shown that CI exists in two forms: a 75 kDa proteolytic repressor form and a 155 kDa activator form. The ratio of these forms, which is regulated positively by hh signaling and negatively by PKA activity, determines the on/off status of hh target gene expression. In this paper, we demonstrate that the exogenous expression of CI that is mutant for four consensus PKA sites [CI(m1-4)], causes ectopic expression of wingless (wg) in vivo and a phenotype consistent with wg overexpression. Expression of CI(m1-4), but not CI(wt), can rescue the hh mutant phenotype and restore wg expression in hh mutant embryos. When PKA activity is suppressed by expressing a dominant negative PKA mutant, the exogenous expression of CI(wt) results in overexpression of wg and lethality in embryogenesis, defects that are similar to those caused by the exogenous expression of CI(m1-4). In addition, we demonstrate that, in cell culture, the mutation of any one of the three serine-containing PKA sites abolishes the proteolytic processing of CI. We also show that PKA directly phosphorylates the four consensus phosphorylation sites in vitro. Taken together, our results suggest that positive hh and negative PKA regulation of wg gene expression converge on the regulation of CI phosphorylation.

scholarly journals Profiling the Abiotic Stress Responsive microRNA Landscape of Arabidopsis thaliana

Plants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 58 ◽  
Author(s):  
Joseph Pegler ◽  
Jackson Oultram ◽  
Christopher Grof ◽  
Andrew Eamens
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Salt Stress ◽  
Abiotic Stress ◽  
Mirna Target ◽  
Target Gene ◽  
Negative Impact ◽  
Mirna Target Gene ◽  
Target Gene Expression ◽  
Response Phenotype

It is well established among interdisciplinary researchers that there is an urgent need to address the negative impacts that accompany climate change. One such negative impact is the increased prevalence of unfavorable environmental conditions that significantly contribute to reduced agricultural yield. Plant microRNAs (miRNAs) are key gene expression regulators that control development, defense against invading pathogens and adaptation to abiotic stress. Arabidopsis thaliana (Arabidopsis) can be readily molecularly manipulated, therefore offering an excellent experimental system to alter the profile of abiotic stress responsive miRNA/target gene expression modules to determine whether such modification enables Arabidopsis to express an altered abiotic stress response phenotype. Towards this goal, high throughput sequencing was used to profile the miRNA landscape of Arabidopsis whole seedlings exposed to heat, drought and salt stress, and identified 121, 123 and 118 miRNAs with a greater than 2-fold altered abundance, respectively. Quantitative reverse transcriptase polymerase chain reaction (RT-qPCR) was next employed to experimentally validate miRNA abundance fold changes, and to document reciprocal expression trends for the target genes of miRNAs determined abiotic stress responsive. RT-qPCR also demonstrated that each miRNA/target gene expression module determined to be abiotic stress responsive in Arabidopsis whole seedlings was reflective of altered miRNA/target gene abundance in Arabidopsis root and shoot tissues post salt stress exposure. Taken together, the data presented here offers an excellent starting platform to identify the miRNA/target gene expression modules for future molecular manipulation to generate plant lines that display an altered response phenotype to abiotic stress.

scholarly journals Deubiquitinase USP47/UBP64E Regulates β-Catenin Ubiquitination and Degradation and Plays a Positive Role in Wnt Signaling

2015 ◽  
Vol 35 (19) ◽  
pp. 3301-3311 ◽  
Author(s):  
Jiandang Shi ◽  
Yajuan Liu ◽  
Xuehe Xu ◽  
Wen Zhang ◽  
Tianxin Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rna Interference ◽  
Wnt Signaling ◽  
Wnt Pathway ◽  
Target Gene ◽  
Central Question ◽  
Cancer Cell Growth ◽  
Positive Role ◽  
Content Type

Wnt signaling plays important roles in development and tumorigenesis. A central question about the Wnt pathway is the regulation of β-catenin. Phosphorylation of β-catenin by CK1α and GSK3 promotes β-catenin binding to β-TrCP, leading to β-catenin degradation through the proteasome. The phosphorylation and ubiquitination of β-catenin have been well characterized; however, it is unknown whether and how a deubiquitinase is involved. In this study, by screening RNA interference (RNAi) libraries, we identified USP47 as a deubiquitinase that prevents β-catenin ubiquitination. Inactivation of USP47 by RNAi increased β-catenin ubiquitination, attenuated Wnt signaling, and repressed cancer cell growth. Furthermore, USP47 deubiquitinates itself, whereas β-TrCP promotes USP47 ubiquitination through interaction with an atypical motif in USP47. Finally,in vivostudies in theDrosophilawing suggest that UBP64E, the USP47 counterpart inDrosophila, is required for Armadillo stabilization and plays a positive role in regulating Wnt target gene expression.

scholarly journals Control of vein-forming, striped gene expression by auxin signaling

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Anmol Krishna ◽  
Jason Gardiner ◽  
Tyler J. Donner ◽  
Enrico Scarpella
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Acetic Acid ◽  
Target Gene ◽  
Target Genes ◽  
Auxin Signaling ◽  
Plant Leaves ◽  
Vein Formation ◽  
Indole 3 Acetic Acid ◽  
Differential Affinity

Abstract Background Activation of gene expression in striped domains is a key building block of biological patterning, from the recursive formation of veins in plant leaves to that of ribs and vertebrae in our bodies. In animals, gene expression is activated in striped domains by the differential affinity of broadly expressed transcription factors for their target genes and the combinatorial interaction between such target genes. In plants, how gene expression is activated in striped domains is instead unknown. We address this question for the broadly expressed MONOPTEROS (MP) transcription factor and its target gene ARABIDOPSIS THALIANA HOMEOBOX FACTOR8 (ATHB8). Results We find that ATHB8 promotes vein formation and that such vein-forming function depends on both levels of ATHB8 expression and width of ATHB8 expression domains. We further find that ATHB8 expression is activated in striped domains by a combination of (1) activation of ATHB8 expression through binding of peak levels of MP to a low-affinity MP-binding site in the ATHB8 promoter and (2) repression of ATHB8 expression by MP target genes of the AUXIN/INDOLE-3-ACETIC-ACID-INDUCIBLE family. Conclusions Our findings suggest that a common regulatory logic controls activation of gene expression in striped domains in both plants and animals despite the independent evolution of their multicellularity.

scholarly journals Control of Vein-Forming, Striped Gene-Expression by Auxin Signaling

2020 ◽  
Author(s):  
Anmol Krishna ◽  
Jason Gardiner ◽  
Tyler J. Donner ◽  
Enrico Scarpella
Keyword(s):  
Gene Expression ◽  
Arabidopsis Thaliana ◽  
Acetic Acid ◽  
Target Gene ◽  
Target Genes ◽  
Auxin Signaling ◽  
Plant Leaves ◽  
Vein Formation ◽  
Indole 3 Acetic Acid ◽  
Differential Affinity

ABSTRACTActivation of gene expression in striped domains is a key building block of biological patterning, from the recursive formation of veins in plant leaves to that of ribs and vertebrae in our bodies. In animals, gene expression is activated in striped domains by the differential affinity of broadly expressed transcription factors for their target genes and the combinatorial interaction between such target genes. In plants, how gene expression is activated in striped domains is instead unknown. We address this question for the broadly expressed MONOPTEROS (MP) transcription factor and its target gene ARABIDOPSIS THALIANA HOMEOBOX FACTOR8 (ATHB8). We find that ATHB8 promotes vein formation and that such vein-forming function depends on both levels of ATHB8 expression and width of ATHB8 expression domains. We further find that ATHB8 expression is activated in striped domains by a combination of (1) activation of ATHB8 expression through binding of peak levels of MP to a low-affinity MP-binding site in the ATHB8 promoter and (2) repression of ATHB8 expression by MP target genes of the INDOLE-3-ACETIC-ACID-INDUCIBLE family such as BODENLOS. Our findings suggest that a common regulatory logic controls activation of gene expression in striped domains in both plants and animals despite the independent evolution of their multicellularity.

Huckebein repressor activity in Drosophila terminal patterning is mediated by Groucho

Development ◽  
1999 ◽  
Vol 126 (17) ◽  
pp. 3747-3755 ◽  
Author(s):  
R.E. Goldstein ◽  
G. Jimenez ◽  
O. Cook ◽  
D. Gur ◽  
Z. Paroush
Keyword(s):  
Gene Expression ◽  
Transcriptional Regulation ◽  
Target Genes ◽  
Developmental Process ◽  
Dna Binding Proteins ◽  
Gap Gene ◽  
Repressor Proteins ◽  
Developmental Contexts ◽  
Repressor Activity

The Groucho corepressor mediates negative transcriptional regulation in association with various DNA-binding proteins in diverse developmental contexts. We have previously implicated Groucho in Drosophila embryonic terminal patterning, showing that it is required to confine tailless and huckebein terminal gap gene expression to the pole regions of the embryo. Here we reveal an additional requirement for Groucho in this developmental process by establishing that Groucho mediates repressor activity of the Huckebein protein. Putative Huckebein target genes are derepressed in embryos lacking maternal groucho activity and biochemical experiments demonstrate that Huckebein physically interacts with Groucho. Using an in vivo repression assay, we identify a functional repressor domain in Huckebein that contains an FRPW tetrapeptide, similar to the WRPW Groucho-recruitment domain found in Hairy-related repressor proteins. Mutations in Huckebein's FRPW motif abolish Groucho binding and in vivo repression activity, indicating that binding of Groucho through the FRPW motif is required for the repressor function of Huckebein. Taken together with our earlier results, these findings show that Groucho-repression regulates sequential aspects of terminal patterning in Drosophila.

scholarly journals Pbx-Hox Heterodimers Recruit Coactivator-Corepressor Complexes in an Isoform-Specific Manner

1999 ◽  
Vol 19 (12) ◽  
pp. 8219-8225 ◽  
Author(s):  
Hiroshi Asahara ◽  
Sanjoy Dutta ◽  
Hung-Ying Kao ◽  
Ronald M. Evans ◽  
Marc Montminy
Keyword(s):  
Gene Expression ◽  
Dna Binding ◽  
Cell Fate ◽  
Target Gene ◽  
Biological Action ◽  
Binding Activity ◽  
Creb Binding Protein ◽  
Target Gene Expression

ABSTRACT Homeobox (hox) proteins have been shown to regulate cell fate and segment identity by promoting the expression of specific genetic programs. In contrast to their restricted biological action in vivo, however, most homeodomain factors exhibit promiscuous DNA binding properties in vitro, suggesting a requirement for additional cofactors that enhance target site selectivity. In this regard, thepbx family of homeobox genes has been found to heterodimerize with and thereby augment the DNA binding activity of certain hox proteins on a subset of potential target sites. Here we examine the transcriptional properties of a forcedhox-pbx heterodimer containing the pancreas-specific orphan homeobox factor pdx fused to pbx-1a. Compared to the pdx monomer, the forced pdx-pbx1a dimer, displayed 10- to 20-fold-higher affinity for a consensushox-pbx binding site but was completely unable to bind ahox monomer recognition site. The pdx-pbx dimer stimulated target gene expression via an N-terminaltrans-activation domain in pdx that interacts with the coactivator CREB binding protein. The pdx-pbxdimer was also found to repress transcription via a C-terminal domain in pbx-1a that associates with the corepressors SMRT and NCoR. The transcriptional properties of the pdx-pbx1complex appear to be regulated at the level of alternative splicing; apdx-pbx polypeptide containing the pbx1bisoform, which lacks the C-terminal extension in pbx1a, was unable to repress target gene expression via NCoR-SMRT. Sincepbx1a and pbx1b are differentially expressed in endocrine versus exocrine compartments of the adult pancreas, our results illustrate a novel mechanism by which pbx proteins may modulate the expression of specific genetic programs, either positively or negatively, during development.

scholarly journals PRDM16 suppresses HIF-targeted gene expression in kidney cancer

2020 ◽  
Vol 217 (6) ◽  
Author(s):  
Anirban Kundu ◽  
Hyeyoung Nam ◽  
Sandeep Shelar ◽  
Darshan S. Chandrashekar ◽  
Garrett Brinkley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Tumor Growth ◽  
Kidney Cancer ◽  
Target Gene ◽  
Physical Interaction ◽  
Gene Encoding ◽  
Functional Studies ◽  
Repressive Effect ◽  
Transcriptional Corepressors

Analysis of transcriptomic data demonstrates extensive epigenetic gene silencing of the transcription factor PRDM16 in renal cancer. We show that restoration of PRDM16 in RCC cells suppresses in vivo tumor growth. RNaseq analysis reveals that PRDM16 imparts a predominantly repressive effect on the RCC transcriptome including suppression of the gene encoding semaphorin 5B (SEMA5B). SEMA5B is a HIF target gene highly expressed in RCC that promotes in vivo tumor growth. Functional studies demonstrate that PRDM16’s repressive properties, mediated by physical interaction with the transcriptional corepressors C-terminal binding proteins (CtBP1/2), are required for suppression of both SEMA5B expression and in vivo tumor growth. Finally, we show that reconstitution of RCC cells with a PRDM16 mutant unable to bind CtBPs nullifies PRDM16’s effects on both SEMA5B repression and tumor growth suppression. Collectively, our data uncover a novel epigenetic basis by which HIF target gene expression is amplified in kidney cancer and a new mechanism by which PRDM16 exerts its tumor suppressive effects.

scholarly journals Differential transcriptional characteristics of small and large biliary epithelial cells derived from small and large bile ducts

2010 ◽  
Vol 299 (3) ◽  
pp. G769-G777 ◽  
Author(s):  
S. Glaser ◽  
M. Wang ◽  
Y. Ueno ◽  
J. Venter ◽  
K. Wang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Epithelial Cells ◽  
Target Gene ◽  
Target Genes ◽  
Biliary Epithelial Cells ◽  
Gene Response ◽  
Before And After ◽  
In Vivo Growth

Biliary epithelial cells (BEC) are morphologically and functionally heterogeneous. To investigate the molecular mechanism for their diversities, we test the hypothesis that large and small BEC have disparity in their target gene response to their transcriptional regulator, the biliary cell-enriched hepatocyte nuclear factor HNF6. The expression of the major HNF ( HNF6, OC2, HNF1b, HNF1a, HNF4a, C/EBPb, and Foxa2) and representative biliary transport target genes that are HNF dependent were compared between SV40-transformed BEC derived from large (SV40LG) and small (SV40SM) ducts, before and after treatment with recombinant adenoviral vectors expressing HNF6 (AdHNF6) or control LacZ cDNA (AdLacZ). Large and small BEC were isolated from mouse liver treated with growth hormone, a known transcriptional activator of HNF6, and the effects on selected target genes were examined. Constitutive Foxa2, HNF1a, and HNF4a gene expression were 2.3-, 12.4-, and 2.6-fold, respectively, higher in SV40SM cells. This was associated with 2.7- and 4-fold higher baseline expression of HNF1a- and HNF4a-regulated ntcp and oatp1 genes, respectively. Following AdHNF6 infection, HNF6 gene expression was 1.4-fold higher ( P = 0.02) in AdHNF6 SV40SM relative to AdHNF6 SV40LG cells, with a corresponding higher Foxa2 (4-fold), HNF1a (15-fold), and HNF4a (6-fold) gene expression in AdHNF6-SV40SM over AdHNF6-SV40LG. The net effects were upregulation of HNF6 target gene glucokinase and of Foxa2, HNF1a, and HNF4a target genes oatp1, ntcp, and mrp2 over AdLacZ control in both cells, but with higher levels in AdH6-SV40SM over AdH6-SV40LG of glucokinase, oatp1, ntcp, and mrp2 (by 1.8-, 3.4-, 2.4-, and 2.5-fold, respectively). In vivo, growth hormone-mediated increase in HNF6 expression was associated with similar higher upregulation of glucokinase and mrp2 in cholangiocytes from small vs. large BEC. Small and large BEC have a distinct profile of hepatocyte transcription factor and cognate target gene expression, as well as differential strength of response to transcriptional regulation, thus providing a potential molecular basis for their divergent function.

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