ABI3
- Known as:
- ABI3
- Catalog number:
- 000956A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABI3
Ask about this productRelated genes to: ABI3
- Gene:
- ABI3 NIH gene
- Name:
- ABI family member 3
- Previous symbol:
- -
- Synonyms:
- NESH, SSH3BP3
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-11
- Date modifiied:
- 2016-10-05
Related products to: ABI3
Related articles to: ABI3
- The regulatory mechanism underlying plant height determination in woody plants remains a long-standing key scientific issue, and the coordinated manner by which positive and negative regulators maintain endogenous hormone homeostasis and modulate final plant architecture is still poorly understood. Here, we identified LfiRAV7 as a pivotal negative regulator of internode elongation in Lagerstroemia indica, providing novel insights into the functional role of APETALA2/Ethylene-Responsive Factor (AP2/ERF) family Related to ABI3/VP1 (RAV) members in governing woody plant architecture. Silencing of LfiRAV7 alleviated its transcriptional repression on plant height-related pathways, resulting in a 43.3% increase in gibberellin (GA) content and a 30.2% reduction in auxin (IAA) abundance, which further facilitated cell division and consequently promoted internode elongation. Protein-protein interaction assays confirmed that LfiRAV7 physically interacts with the positive regulator LfiGI (GIGANTEA). Silencing of LfiGI suppressed GA biosynthesis and inhibited both cell division and expansion. Integrated multi-omics analysis combining DAP-seq and RNA-seq demonstrated that LfiRAV7 did not exert widespread effects on metabolic pathways; instead, it directly bound to the E-box motif of LfiGA3ox, encoding the terminal rate-limiting enzyme of the GA biosynthesis pathway, and repressed its transcription. Collectively, we uncovered an antagonistic regulatory module consisting of LfiRAV7 and LfiGI, which not only revealed a previously uncharacterized genetic mechanism underlying the regulation of endogenous hormone homeostasis and morphogenesis in woody plants, but also offered key candidate targets for directed creation of ideal plant architecture in woody ornamental species. - Source: PubMed
Wang XinChi XiufengMa TianxiaoXu YingnaShen PingWan ZhitingLin QifangJu YiqianWang HuanCai MingWang JiaCheng TangrenZhang QixiangPan Huitang - The splicing of group Ⅱ introns in chloroplasts is essential for photosynthesis and plant development and relies on a series of nucleus-encoded RNA-binding proteins. Here, we demonstrate that two Arabidopsis proteins, ribonuclease Ⅲ-domain protein AtRNC1 and the Plant organelle RNA recognition (PORR) protein AtWTF1, are essential for chloroplast function. Null mutants of AtRNC1 or AtWTF1 are embryo lethal. We rescued the null mutant by expressing wild-type AtRNC1 under the control of the seed-specific ABSCISIC ACID-INSENSITIVE3 (ABI3) promoter. We also created atrnc1 knockdown plants using artificial-microRNA (amiRNA). Both the rescued and knockdown atrnc1 plants exhibit chlorotic phenotype. Similarly, AtWTF1 hypomorphic mutants display variegated phenotypes. Both proteins are chloroplast-localized, with AtRNC1 residing in the stroma and AtWTF1 in both the stroma and thylakoids. Molecular phenotyping established that AtRNC1 and AtWTF1 are required for the efficient splicing of a specific, overlapping set of chloroplast group Ⅱ introns, including those in petB, petD, rpl2, rps12, and tRNAs. RNA immunoprecipitation confirmed the association of both proteins with their target introns in vivo, indicating direct roles in splicing. The knockdown of AtRNC1 or AtWTF1 in Arabidopsis impairs the chloroplast ribosome accumulation and accordingly reduced the efficiency of mRNA translation. Notably, protein interaction assays, including yeast two-hybrid, luciferase complementation image, and IP-MS indicate that AtRNC1 and AtWTF1 associate with each other, implying their cooperative function in a splicing complex. These findings establish AtRNC1 and AtWTF1 as key components of the chloroplast RNA splicing machinery, essential for the maturation of plastid transcripts and overall chloroplast homeostasis in Arabidopsis. - Source: PubMed
Publication date: 2026/08/24
Zhang YichenXu XinyunLi YajuanWei SiwenShen JiayiYu Qing-BoCui Yong-Lan - Pentatricopeptide repeat (PPR) proteins are key regulators of the organellar RNA metabolism in plants. However, the functions of mitochondrial PPR proteins belonging to the subclass of P-type PPR factors containing the SMR domain remain much less understood. Here, we characterize the EMBRYO DEFECTIVE 2217 (EMB2217/At1g79490), an essential PPR-SMR factor in Arabidopsis thaliana. T-DNA insertional lines at the AT1G79490 gene-locus exhibit embryonic arrest at the late heart stage and display defective germination and seedling establishment. Partial complementation using an ABI3 promoter-driven strategy enables efficient germination and the rescue of homozygous emb2217 plantlets. The pABI3::EMB2217 emb2217 -/- seedlings display severe growth defects due to impaired mitochondrial function, tightly associated with impaired OXPHOS activity. Analyses of mitochondrial RNA profiles reveal that EMB2217 is required for the processing of multiple group II introns that reside in the coding regions of several complex I (CI) subunits, the cox2 subunit of CIV, and the ribosomal rps3 factors. Our data further show that RNA maturation defects induce alternative electron transport and stress-response pathways, which are associated with developmental defects and modulation of photosynthetic and cellular metabolic processes. Together, we identify EMB2217 as a general mitochondrial splicing factor whose loss compromises OXPHOS biogenesis and function, cellular energy supply, and plant development. - Source: PubMed
Marchetti FernandaBalestieri NehuenBecerra-Agudelo EvelynValiñas MatíasAmigo NataliaMatan RoeiMizrahi RonTakenaka MizukiWelchen ElinaPagnussat Gabriela CarolinaOstersetzer-Biran OrenZabaleta Eduardo - Gibberellins (GAs) are central regulators of plant growth and development, yet their involvement in somatic embryogenesis (SE) has received limited attention and often produces contradictory results. This review critically examines the current knowledge on the role of GAs in SE by integrating evidence from physiological, molecular, and developmental studies across a wide range of plant species. Available data indicate that exogenous GAs and GA biosynthesis inhibitors can either promote or inhibit the induction, progression, and conversion of somatic embryos, depending on the species, genotype, explant origin, developmental stage, and culture conditions. These opposing effects underscore that exogenous responses are tightly linked to endogenous GA homeostasis. Particular attention is paid to GA metabolism and signaling genes, whose expression patterns during SE reveal substantial interspecific and genotypic variation. Endogenous GA profiles reveal that both high and low levels of bioactive GAs correlate with SE induction across different systems, suggesting that endogenous GA levels may be a key determinant of embryogenic competence and may underlie major differences in regeneration capacity among species and genotypes. Furthermore, GAs function within a broader regulatory network through extensive crosstalk with other hormones (auxins, abscisic acid, cytokinins, and ethylene), environmental factors (e.g., light and temperature) and interactions with major embryogenesis-related transcription factors such as LEC1, LEC2, FUS3, ABI3, AGL15, AGL18, and BBM. These interactions position GAs as dynamic components of a multilayered hormonal and transcriptional framework that controls the switch from somatic to embryogenic development. Integrative approaches-including hormone profiling, gene expression analysis, functional genetics, and developmental studies-are essential to elucidate the precise function of GAs in SE and thereby improve protocols for plant regeneration. - Source: PubMed
Publication date: 2026/07/27
Belić MajaZdravković-Korać SnežanaMilojević Jelena - A total of 164 APETALA2/ethylene-responsive factor (AP2/ERF) genes were identified in Hydrangea macrophylla, and HmaERF87 positively contributes to leaf spot resistance. The APETALA2/ethylene-responsive factor (AP2/ERF) transcription factor family plays important roles in plant stress responses, but its contribution to disease resistance in Hydrangea macrophylla (hydrangea) remains poorly understood. In this study, 164 AP2/ERF genes were identified in the H. macrophylla genome and classified into APETALA2 (AP2), ethylene-responsive factor (ERF), dehydration-responsive element-binding (DREB), and related to ABI3/VP1 (RAV) subfamilies. Their chromosomal distribution, conserved motifs, gene structures, and duplication patterns were analyzed. A total of 46 pathogen-responsive H. macrophylla AP2/ERF (HmaERF) genes were identified from the RNA sequencing (RNA-seq) dataset of resistant and susceptible cultivar leaves collected before and after Corynespora cassiicola inoculation. Promoter analysis revealed that the HmaERF genes with upregulated expression post-C. cassiicola infection showed a higher frequency and copy number of jasmonate-responsive cis-regulatory elements, suggesting their possible involvement in hormone-mediated defense responses. Three infection-induced candidate genes, including HmaERF56, HmaERF87, and HmaERF129, were selected for functional validation using virus-induced gene silencing (VIGS) in hydrangea leaf discs. Silencing of HmaERF87 expression via VIGS significantly increased lesion development after C. cassiicola inoculation, whereas the transient overexpression of HmaERF87 reduced the area of leaf disc lesions. Subcellular localization showed that the HmaERF87 protein was localized in the nucleus, and yeast assays indicated that its transcriptional activation activity was mainly associated with the C-terminal region of the protein. These results support a role for HmaERF87 as a positive regulator of H. macrophylla resistance to leaf spot disease and provide a candidate gene for further studies of disease resistance in hydrangea. - Source: PubMed
Publication date: 2026/08/07
Chen ShuyuanLiu XintongZhang ChengweiZhang ZiqinChen HuijieHan YongChen ShuangshuangFeng JingWang GuanglingLi ChangWu ZedongDeng Yanming