PACLOBUTRAZOL-RESISTANCE Gene Family Regulates Floral Organ Growth with Unequal Genetic Redundancy in Arabidopsis thaliana.
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ABSTRACT:
SUBMITTER: Shin K
PROVIDER: S-EPMC6412927 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Abscission is a developmental program that results in the active shedding of infected or nonfunctional organs from a plant body. Here, we establish a signaling pathway that controls abscission in Arabidopsis thaliana from ligand, to receptors, to downstream effectors. Loss of function mutations in Inflorescence Deficient in Abscission (IDA), which encodes a predicted secreted small protein, the receptor-like protein kinases HAESA (HAE) and HAESA-like 2 (HSL2), the Mitogen-Activated Protein Kinase Kinase 4 (MKK4) and MKK5, and a dominant-negative form of Mitogen-Activated Protein Kinase 6 (MPK6) in a mpk3 mutant background all have abscission-defective phenotypes. Conversely, expression of constitutively active MKKs rescues the abscission-defective phenotype of hae hsl2 and ida plants. Additionally, in hae hsl2 and ida plants, MAP kinase activity is reduced in the receptacle, the part of the stem that holds the floral organs. Plants overexpressing IDA in a hae hsl2 background have abscission defects, indicating HAE and HSL2 are epistatic to IDA. Taken together, these results suggest that the sequential action of IDA, HAE and HSL2, and a MAP kinase cascade regulates the programmed separation of cells in the abscission zone.
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Project description:Voltage-dependent anion channels (VDACs) are the most important proteins in mitochondria. They localize to the outer mitochondrial membrane and contribute to the metabolite transport between the mitochondria and cytoplasm, which aids plant growth regulation. Here, we report that Arabidopsis thaliana VDAC1 is involved in the floral transition, with the loss of AtVDAC1 function, resulting in an early-flowering phenotype. AtVDAC1 is expressed ubiquitously in Arabidopsis. To identify the flowering pathway integrators that may be responsible for AtVDAC1's function during the floral transition, an RNA-seq analysis was performed. In total, 106 differentially expressed genes (DEGs) were identified between wild-type and atvdac1-5 mutant seedlings. However, none were involved in flowering-related pathways. In contrast, AtVDAC1 physically associated with FLOWERING LOCUS T. Thus, in the floral transition, AtVDAC1 may function partly through the FLOWERING LOCUS T protein.
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Project description:Flowering is one of the important defining features of angiosperms. The initiation of flower development and the formation of different floral organs are the results of the interplays among numerous genes. But until now, just fewer genes have been found linked with flower development. And the functions of lots of genes of Arabidopsis thaliana are still unknown. Although, the quartet model successfully simplified the ABCDE model to elaborate the molecular mechanism by introducing protein-protein interactions (PPIs). We still don't know much about several important aspects of flower development. So we need to discriminate even more genes involving in the flower development. In this study, we identified seven differentially modules through integrating the weighted gene co-expression network analysis (WGCNA) and Support Vector Machine (SVM) method to analyze co-expression network and PPIs using the public floral and non-floral expression profiles data of Arabidopsis thaliana. Gene set enrichment analysis was used for the functional annotation of the related genes, and some of the hub genes were identified in each module. The potential floral organ morphogenesis genes of two significant modules were integrated with PPI information in order to detail the inherent regulation mechanisms. Finally, the functions of the floral patterning genes were elucidated by combining the PPI and evolutionary information. It was indicated that the sub-networks or complexes, rather than the genes, were the regulation unit of flower development. We found that the most possible potential new genes underlining the floral pattern formation in A. thaliana were FY, CBL2, ZFN3, and AT1G77370; among them, FY, CBL2 acted as an upstream regulator of AP2; ZFN3 activated the flower primordial determining gene AP1 and AP2 by HY5/HYH gene via photo induction possibly. And AT1G77370 exhibited similar function in floral morphogenesis, same as ELF3. It possibly formed a complex between RFC3 and RPS15 in cytoplasm, which regulated TSO1 and CPSF160 in the nucleus, to control the floral organ morphogenesis. This process might also be fine tuning by AT5G53360 in the nucleus.
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Project description:BackgroundThe proteasome subunit RPT5, which is essential for gametophyte development, is encoded by two genes in Arabidopsis thaliana; RPT5a and RPT5b. We showed previously that RPT5a and RPT5b are fully redundant in the Columbia (Col-0) accession, whereas in the Wassilewskia accession (Ws-4), RPT5b does not complement the effect of a strong rpt5a mutation in the male gametophyte, and only partially complements rpt5a mutation in the sporophyte. RPT5bCol-0 and RPT5bWs-4 differ by only two SNPs, one located in the promoter and the other in the seventh intron of the gene.ResultsBy exploiting natural variation at RPT5b we determined that the SNP located in RPT5b intron seven, rather than the promoter SNP, is the sole basis of this lack of redundancy. In Ws-4 this SNP is predicted to create a new splicing branchpoint sequence that induces a partial mis-splicing of the pre-mRNA, leading to the introduction of a Premature Termination Codon. We characterized 5 accessions carrying this A-to-T substitution in intron seven and observed a complete correlation between this SNP and both a 10 to 20% level of the RPT5b pre-mRNA mis-splicing and the lack of ability to complement an rpt5a mutant phenotype.ConclusionThe accession-dependent unequal redundancy between RPT5a and RPT5b genes illustrates an example of evolutionary drifting between duplicated genes through alternative splicing.
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Project description:BackgroundRACK1 is a versatile scaffold protein in mammals, regulating diverse developmental processes. Unlike in non-plant organisms where RACK1 is encoded by a single gene, Arabidopsis genome contains three RACK1 homologous genes, designated as RACK1A, RACK1B and RACK1C, respectively. Previous studies indicated that the loss-of-function alleles of RACK1A displayed multiple defects in plant development. However, the functions of RACK1B and RACK1C remain elusive. Further, the relationships between three RACK1 homologous genes are unknown.ResultsWe isolated mutant alleles with loss-of-function mutations in RACK1B and RACK1C, and examined the impact of these mutations on plant development. We found that unlike in RACK1A, loss-of-function mutations in RACK1B or RACK1C do not confer apparent defects in plant development, including rosette leaf production and root development. Analyses of rack1a, rack1b and rack1c double and triple mutants, however, revealed that rack1b and rack1c can enhance the rack1a mutant's developmental defects, and an extreme developmental defect and lethality were observed in rack1a rack1b rack1c triple mutant. Complementation studies indicated that RACK1B and RACK1C are in principle functionally equivalent to RACK1A. Gene expression studies indicated that three RACK1 genes display similar expression patterns but are expressed at different levels. Further, RACK1 genes positively regulate each other's expression.ConclusionThese results suggested that RACK1 genes are critical regulators of plant development and that RACK1 genes function in an unequally redundant manner. Both the difference in RACK1 gene expression level and the cross-regulation are likely the molecular determinants of their unequal genetic redundancy.
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Project description:Abscission is a developmental process that enables plants to shed unwanted organs. In Arabidopsis, the floral organ abscission is regulated by a signaling pathway consisting of the peptide ligand IDA, the receptor-like kinases (RLKs) HAE and HSL2, and a downstream MAP kinase (MAPK) cascade. However, little is known about the molecular link between ligand-receptor pairs and intracellular signaling. Here, we report that the SERK family RLKs function redundantly in regulating floral organ abscission downstream of IDA and upstream of the MAPK cascade. IDA induces heterodimerization of HAE/HSL2 and SERKs, which transphosphorylate each other. The SERK3 residues mediating its interaction with the immune receptor FLS2 and the brassinosteroid receptor BRI1 are also required for IDA-induced HAE/HSL2-SERK3 interaction, suggesting SERKs serve as co-receptors of HAE/HSL2 in perceiving IDA. Thus, our study reveals the signaling activation mechanism in floral organ abscission by IDA-induced HAE/HSL2-SERK complex formation accompanied by transphosphorylation.
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Project description:Organismal development is remarkably robust, tolerating stochastic errors to produce consistent, so-called canalized adult phenotypes. The mechanistic underpinnings of developmental robustness are poorly understood, but recent studies implicate certain features of genetic networks such as functional redundancy, connectivity, and feedback. Here, we examine the BZR/BEH gene family, whose function contributes to embryonic stem development in the plant Arabidopsis thaliana, to test current assumptions on functional redundancy and trait robustness. Our analyses of BZR/BEH gene mutants and mutant combinations revealed that functional redundancy among these gene family members is not necessary for trait robustness. Connectivity is another commonly cited determinant of robustness; however, we found no correlation between connectivity among gene family members or their connectivity with other transcription factors and effects on developmental robustness. Instead, our data suggest that BEH4, the earliest diverged family member, modulates developmental robustness. We present evidence indicating that regulatory cross-talk among gene family members is integrated by BEH4 to promote wild-type levels of developmental robustness. Further, the chaperone HSP90, a known determinant of developmental robustness, appears to act via BEH4 in maintaining robustness of embryonic stem length. In summary, we demonstrate that even among closely related transcription factors, trait robustness can arise through the activity of a single gene family member, challenging common assumptions about the molecular underpinnings of robustness.
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Project description:KEY MESSAGE:Linear modelling approaches detected significant gradients in organ growth and patterning across early flowers of the Arabidopsis inflorescence and uncovered evidence of new roles for gibberellin in floral development. Most flowering plants, including the genetic model Arabidopsis thaliana, produce multiple flowers in sequence from a reproductive shoot apex to form a flower spike (inflorescence). The development of individual flowers on an Arabidopsis inflorescence has typically been considered as highly stereotypical and uniform, but this assumption is contradicted by the existence of mutants with phenotypes visible in early flowers only. This phenomenon is demonstrated by mutants partially impaired in the biosynthesis of the phytohormone gibberellin (GA), in which floral organ growth is retarded in the first flowers to be produced but has recovered spontaneously by the 10th flower. We presently lack systematic data from multiple flowers across the Arabidopsis inflorescence to explain such changes. Using mutants of the GA 20-OXIDASE (GA20ox) GA biosynthesis gene family to manipulate endogenous GA levels, we investigated the dynamics of changing floral organ growth across the early Arabidopsis inflorescence (flowers 1-10). Modelling of floral organ lengths identified a significant, GA-independent gradient of increasing stamen length relative to the pistil in the wild-type inflorescence that was separable from other, GA-dependent effects. It was also found that the first flowers exhibited unstable organ patterning in contrast to later flowers and that this instability was prolonged by exogenous GA treatment. These findings indicate that the development of individual flowers is influenced by hitherto unknown factors acting across the inflorescence and also suggest novel functions for GA in floral patterning.
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Project description:Genetic redundancy refers to a situation where an individual with a loss-of-function mutation in one gene (single mutant) does not show an apparent phenotype until one or more paralogs are also knocked out (double/higher-order mutant). Previous studies have identified some characteristics common among redundant gene pairs, but a predictive model of genetic redundancy incorporating a wide variety of features derived from accumulating omics and mutant phenotype data is yet to be established. In addition, the relative importance of these features for genetic redundancy remains largely unclear. Here, we establish machine learning models for predicting whether a gene pair is likely redundant or not in the model plant Arabidopsis thaliana based on six feature categories: functional annotations, evolutionary conservation including duplication patterns and mechanisms, epigenetic marks, protein properties including posttranslational modifications, gene expression, and gene network properties. The definition of redundancy, data transformations, feature subsets, and machine learning algorithms used significantly affected model performance based on holdout, testing phenotype data. Among the most important features in predicting gene pairs as redundant were having a paralog(s) from recent duplication events, annotation as a transcription factor, downregulation during stress conditions, and having similar expression patterns under stress conditions. We also explored the potential reasons underlying mispredictions and limitations of our studies. This genetic redundancy model sheds light on characteristics that may contribute to long-term maintenance of paralogs, and will ultimately allow for more targeted generation of functionally informative double mutants, advancing functional genomic studies.
| S-EPMC8321531 | biostudies-literature
Project description:The floral developmental pathway in Arabidopsis thaliana is composed of several interacting regulatory genes, including the inflorescence architecture gene TERMINAL FLOWER1 (TFL1), the floral meristem identity genes LEAFY (LFY), APETALA1 (AP1), and CAULIFLOWER (CAL), and the floral organ identity genes APETALA3 (AP3) and PISTILLATA (PI). Molecular population genetic analyses of these different genes indicate that the coding regions of AP3 and PI, as well as AP1 and CAL, share similar levels and patterns of nucleotide diversity. In contrast, the coding regions of TFL1 and LFY display a significant reduction in nucleotide variation, suggesting that these sequences have been subjected to a recent adaptive sweep. Moreover, the promoter of TFL1, unlike its coding region, displays high levels of diversity organized into two distinct haplogroups that appear to be maintained by selection. These results suggest that patterns of molecular evolution differ among regulatory genes in this developmental pathway, with the earlier acting genes exhibiting evidence of adaptive evolution.
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