Browse
Submit Data
Databases
API
Help

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

OsRELA Regulates Leaf Inclination by Repressing the Transcriptional Activity of OsLIC in Rice

ABSTRACT: Leaf angle is one of the most important agronomic traits in rice, and changes in leaf angle can alter plant architecture to affect photosynthetic efficiency and thus determine grain yield. Therefore, it is important to identify key genes controlling leaf angle and elucidate the molecular mechanisms to improve rice yield. We obtained a mutant rela (regulator of leaf angle) with reduced leaf angle in rice by EMS mutagenesis, and map-based cloning revealed that OsRELA encodes a protein of unknown function. Coincidentally, DENSE AND ERECT PANICLE 2 (DEP2) was reported in a previous study with the same gene locus. RNA-seq analysis revealed that OsRELA is involved in regulating the expression of ILI and Expansin family genes. Biochemical and genetic analyses revealed that OsRELA is able to interact with OsLIC, a negative regulator of BR signaling, through its conserved C-terminal domain, which is essential for OsRELA function in rice. The binding of OsRELA can activate the expression of downstream genes repressed by OsLIC, such as OsILI1, a positive regulator of leaf inclination in rice. Therefore, our results suggest that OsRELA can act as a transcriptional regulator and is involved in the regulation of leaf inclination by regulating the transcriptional activity of OsLIC.

SUBMITTER: Zhu C

PROVIDER: S-EPMC8519309 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Similar Datasets

SPOC domain-containing protein Leaf inclination3 interacts with LIP1 to regulate rice leaf inclination through auxin signaling.

Project description:Leaf angle is an important agronomic trait and influences crop architecture and yield. Studies have demonstrated the roles of phytohormones, particularly auxin and brassinosteroids, and various factors in controlling leaf inclination. However, the underlying mechanism especially the upstream regulatory networks still need being clarified. Here we report the functional characterization of rice leaf inclination3 (LC3), a SPOC domain-containing transcription suppressor, in regulating leaf inclination through interacting with LIP1 (LC3-interacting protein 1), a HIT zinc finger domain-containing protein. LC3 deficiency results in increased leaf inclination and enhanced expressions of OsIAA12 and OsGH3.2. Being consistent, transgenic plants with OsIAA12 overexpression or deficiency of OsARF17 which interacts with OsIAA12 do present enlarged leaf inclination. LIP1 directly binds to promoter regions of OsIAA12 and OsGH3.2, and interacts with LC3 to synergistically suppress auxin signaling. Our study demonstrate the distinct effects of IAA12-ARF17 interactions in leaf inclination regulation, and provide informative clues to elucidate the functional mechanism of SPOC domain-containing transcription suppressor and fine-controlled network of lamina joint development by LC3-regulated auxin homeostasis and auxin signaling through.

| S-EPMC6289470 | biostudies-literature

Arabidopsis STO/BBX24 negatively regulates UV-B signaling by interacting with COP1 and repressing HY5 transcriptional activity.

Project description:UV-B (280-315 nm) is an integral part of solar radiation and can act either as a stress inducer or as a developmental signal. In recent years, increasing attention has been paid to the low-fluence UV-B-induced photomorphogenic response and several key players in this response have been identified, which include UVR8 (a UV-B-specific photoreceptor), COP1 (a WD40-repeat-containing RING finger protein), HY5 (a basic zipper transcription factor), and RUP1/2 (two UVR8-interacting proteins). Here we report that Arabidopsis SALT TOLERANCE (STO/BBX24), a known regulator for light signaling in plants, defines a new signaling component in UV-B-mediated photomorphogenesis. The bbx24 mutant is hypersensitive to UV-B radiation and becomes extremely dwarfed under UV-B treatment. By contrast, BBX24 overexpression transgenic lines respond much more weakly to UV-B than the bbx24 and wild-type plants. BBX24 expression is UV-B-inducible and its accumulation under UV-B requires COP1. Co-immunoprecipitation experiments indicate that BBX24 interacts with COP1 in planta upon UV-B illumination. Moreover, BBX24 interacts with HY5 and acts antagonistically with HY5 in UV-B-induced inhibition of hypocotyl elongation. Furthermore, BBX24 attenuates UV-B-induced HY5 accumulation and suppresses its transcription-activation activity. Taken together, our results reveal a previously uncharacterized function of the light-regulated BBX24 in UV-B responses and demonstrate that BBX24 functions as a negative regulator of photomorphogenic UV-B responses by interacting with both COP1 and HY5. The UV-B-inducible expression pattern and its suppression of HY5 activity suggest that BBX24 could be a new component of the feedback regulatory module of UV-B signaling in plants.

| S-EPMC3367526 | biostudies-literature

The transcriptional co-repressor TLE3 regulates myogenic differentiation by repressing the activity of the MyoD transcription factor.

Project description:Satellite cells are skeletal muscle stem cells that provide myonuclei for postnatal muscle growth, maintenance, and repair/regeneration in adults. Normally, satellite cells are mitotically quiescent, but they are activated in response to muscle injury, in which case they proliferate extensively and exhibit up-regulated expression of the transcription factor MyoD, a master regulator of myogenesis. MyoD forms a heterodimer with E proteins through their basic helix-loop-helix domain, binds to E boxes in the genome and thereby activates transcription at muscle-specific promoters. The central role of MyoD in muscle differentiation has increased interest in finding potential MyoD regulators. Here we identified transducin-like enhancer of split (TLE3), one of the Groucho/TLE family members, as a regulator of MyoD function during myogenesis. TLE3 was expressed in activated and proliferative satellite cells in which increased TLE3 levels suppressed myogenic differentiation, and, conversely, reduced TLE3 levels promoted myogenesis with a concomitant increase in proliferation. We found that, via its glutamine- and serine/proline-rich domains, TLE3 interferes with MyoD function by disrupting the association between the basic helix-loop-helix domain of MyoD and E proteins. Our findings indicate that TLE3 participates in skeletal muscle homeostasis by dampening satellite cell differentiation via repression of MyoD transcriptional activity.

| S-EPMC5546029 | biostudies-literature

Dataset of leaf inclination angles for 71 different Eucalyptus species.

Project description:The leaf inclination angle distribution is an important parameter in models useful for understanding forest canopy processes of photosynthesis, evapotranspiration, radiation transmission, and spectral reflectance. Yet, despite the strong sensitivity of many of these models to variability in leaf inclination angle distribution, relatively few measurements have been reported for different tree species in literature and databases such as TRY, and various assumptions about leaf inclination angle distribution are often made by modellers. Here we provide a dataset of leaf inclination angles for 71 different Australia-native Eucalyptus species measured in 13 botanical gardens around the world. Leaf inclination angles were measured using a leveled digital camera approach. The leaf angle measurements were used to estimate corresponding Beta distribution parameters and to assign the appropriate classic type of leaf inclination angle distribution. The data can be used to parameterize leaf angle distributions in e.g., physically-based reflectance models, land surface models, and regional carbon cycle models.

| S-EPMC7569295 | biostudies-literature

VIRESCENT-ALBINO LEAF 1 regulates leaf colour development and cell division in rice.

Project description:The de novo synthesis of purine nucleotides is crucial to all living organisms, but limited information is available for plants. In this study, we isolated a virescent-albino leaf 1 (val1) mutant of rice (Oryza sativa) that produces dynamic green-revertible albino and narrow-leaf phenotypes. In albino leaves, chloroplast development was defective, pigment contents were reduced, and cell division was impaired compared with the wild-type. Map-based cloning revealed that VAL1 encodes a phosphoribosylamine-glycine ligase (PurD), the second enzyme in the de novo purine biosynthesis pathway. Subcellular localization analysis demonstrated that VAL1 was localized in the chloroplast. Our results demonstrate that VAL1 is a crucial enzyme in the de novo purine biosynthesis pathway and is involved in regulating chloroplast development, chlorophyll metabolism, and cell division during leaf development in rice.

| S-EPMC6137968 | biostudies-literature

Hexokinase gene OsHXK1 positively regulates leaf senescence in rice.

Project description:BackgroundLeaf senescence is a highly complex and meticulous regulatory process, and the disruption of any factor involved in leaf senescence might lead to premature or delayed leaf senescence and thus result in reduced or increased crop yields. Despite sincere efforts by scientists, there remain many unsolved problems related to the regulatory factors and molecular mechanisms of leaf senescence.ResultsThis study successfully revealed that OsHXK1 was highly expressed in senescent leaves of rice. The upregulation of OsHXK1 led to premature senescence of rice leaves, a decreased level of chlorophyll, and damage to the chloroplast structure. The overexpression of OsHXK1 resulted in increases in glucose and ROS levels and produced programmed cell death (PCD) signals earlier at the booting stage. Further analysis showed that expression level of the respiratory burst oxidase homolog (RBOH) genes and OsGLO1 were increased in OsHXK1-overexpressing plants at the booting stage.ConclusionsOverall, the outcomes of this study suggested that OsHXK1 could act as a positive regulator of rice leaf senescence by mediating glucose accumulation and inducing an increase in ROS.

| S-EPMC8653616 | biostudies-literature

Homeobox A4 suppresses vascular remodeling by repressing YAP/TEAD transcriptional activity.

Project description:The Hippo signaling pathway is involved in the pathophysiology of various cardiovascular diseases. Yes-associated protein (YAP) and transcriptional enhancer activator domain (TEAD) transcriptional factors, the main transcriptional complex of the Hippo pathway, were recently identified as modulators of phenotypic switching of vascular smooth muscle cells (VSMCs). However, the intrinsic regulator of YAP/TEAD-mediated gene expressions involved in vascular pathophysiology remains to be elucidated. Here, we identified Homeobox A4 (HOXA4) as a potent repressor of YAP/TEAD transcriptional activity using lentiviral shRNA screen. Mechanistically, HOXA4 interacts with TEADs and attenuates YAP/TEAD-mediated transcription by competing with YAP for TEAD binding. We also clarified that the expression of HOXA4 is relatively abundant in the vasculature, especially in VSMCs. In vitro experiments in human VSMCs showed HOXA4 maintains the differentiation state of VSMCs via inhibition of YAP/TEAD-induced phenotypic switching. We generated Hoxa4-deficient mice and confirmed the downregulation of smooth muscle-specific contractile genes and the exacerbation of vascular remodeling after carotid artery ligation in vivo. Our results demonstrate that HOXA4 is a repressor of VSMC phenotypic switching by inhibiting YAP/TEAD-mediated transcription.

| S-EPMC7132199 | biostudies-literature

MRF4 negatively regulates adult skeletal muscle growth by repressing MEF2 activity

Project description:The myogenic regulatory factor MRF4 is expressed at high levels in myofibers of adult skeletal muscle, but its function is unknown. Here we show that knockdown of MRF4 in adult muscle causes hypertrophy and prevents denervation-induced atrophy. This effect is accompanied by increased protein synthesis and the widespread activation of genes involved in muscle contraction, excitation-contraction coupling and energy metabolism, many of which are known targets of MEF2 transcription factors. Genes regulated by MEF2 represent the top-ranking gene set enriched after Mrf4 RNAi, and a MEF2 reporter is inhibited by co-transfected MRF4 and activated by Mrf4 RNAi. The role of MEF2 in mediating the effect of MRF4 knockdown is supported by the finding that Mrf4 RNAi-dependent increase in fiber size is prevented by dominant negative MEF2, while constitutively active MEF2 is able to induce myofiber hypertrophy. The nuclear localization of the MEF2 co-repressor HDAC4 is impaired by Mrf4 knockdown, suggesting that MRF4 acts by stabilizing a repressor complex that controls MEF2 activity. The demonstration that fiber size in adult skeletal muscle is controlled by the MRF4-MEF2 axis opens new perspectives in the search for therapeutic targets to prevent muscle wasting, in particular sarcopenia and cachexia. Adult innervated and denervated rat soleus muscles were transfected with shRNA to Mrf4 (M1) or to LacZ as a control. Muscles were dissected and examined after 7 days. For each group/condition we selected three different muscles (biological replicas).

2016-07-15 | E-GEOD-67069 | biostudies-arrayexpress

Ribosomal RACK1 Regulates the Dendritic Arborization by Repressing FMRP Activity.

Project description:FMRP is an RNA-binding protein that represses the translation of specific mRNAs. In neurons, its depletion determines the exaggerated translation of mRNAs leading to dendritic and axonal aberrant development, two peculiar features of Fragile X syndrome patients. However, how FMRP binds to translational machinery to regulate the translation of its mRNA targets is not yet fully understood. Here, we show that FMRP localizes on translational machinery by interacting with the ribosomal binding protein, Receptor for Activated C Kinase 1 (RACK1). The binding of FMRP to RACK1 removes the translational repressive activity of FMRP and promotes the translation of PSD-95 mRNA, one specific target of FMRP. This binding also results in a reduction in the level of FMRP phosphorylation. We also find that the morphological abnormalities induced by Fmr1 siRNA in cortical neurons are rescued by the overexpression of a mutant form of RACK1 that cannot bind ribosomes. Thus, these results provide a new mechanism underlying FMRP activity that contributes to altered development in FXS. Moreover, these data confirm the role of ribosomal RACK1 as a ribosomal scaffold for RNA binding proteins.

| S-EPMC9569565 | biostudies-literature

Narrow and Stripe Leaf 2 Regulates Leaf Width by Modulating Cell Cycle Progression in Rice.

Project description:BackgroundLeaf morphology is an important component of the idea plant architecture that extensively influences photosynthesis, transpiration, and ultimately grain yield in crops. However, the genetic and molecular mechanisms regulating this morphology remain largely unclear.ResultsIn this study, a mutant showing a narrow and stripe leaf phonotype, designated nsl2, was obtained. Histological analysis revealed defects in the vascular system and reduced epidermal cell number in the nsl2, while the cell size remained unchanged. Map-based cloning and genetic complementation experiments revealed that NSL2, which encodes a small subunit of ribonucleotide reductases (RNRs), is a null allelic with ST1 and SDL. The NSL2 was expressed in variety of tissues, with the highest levels detected in leaves, and its protein was localized in the nucleus and cytoplasm. The dNTPs level was altered in the nsl2 mutant, and thereby affecting the dNTPs pool balance. In addition, flow cytometric analysis and the altered transcript level of genes related to cell cycle indicated that NSL2 affects cell cycle progression.ConclusionsOur findings here suggest that NSL2 function in the synthesis of dNTP, the deficient of which leads to DNA synthesis block and in turn affects cell cycle progression, and ultimately decreased cell number and narrow leaf in the nsl2 plant.

| S-EPMC10113404 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data