scholarly journals The structure and activity of nodulation-suppressing CLE peptide hormones of legumes

2015 ◽  
Vol 42 (3) ◽  
pp. 229 ◽  
Author(s):  
April H. Hastwell ◽  
Peter M. Gresshoff ◽  
Brett J. Ferguson
Keyword(s):  
Molecular Mechanisms ◽  
De Novo ◽  
Lotus Japonicus ◽  
Peptide Hormones ◽  
Negative Feedback Loops ◽  
C Terminus ◽  
Cle Peptides ◽  
Autoregulation Of Nodulation ◽  
Cle Peptide ◽  
External Stimuli

Legumes form a highly-regulated symbiotic relationship with specific soil bacteria known as rhizobia. This interaction results in the de novo formation of root organs called nodules, in which the rhizobia fix atmospheric di-nitrogen (N2) for the plant. Molecular mechanisms that regulate the nodulation process include the systemic ‘autoregulation of nodulation’ and the local nitrogen-regulation of nodulation pathways. Both pathways are mediated by novel peptide hormones called CLAVATA/ESR-related (CLE) peptides that act to suppress nodulation via negative feedback loops. The mature peptides are 12–13 amino acids in length and are post-translationally modified from the C-terminus of tripartite-domain prepropeptides. Structural redundancy between the prepropeptides exists; however, variations in external stimuli, timing of expression, tissue specificity and presence or absence of key functional domains enables them to act in a specific manner. To date, nodulation-regulating CLE peptides have been identified in Glycine max (L.) Merr., Medicago truncatula Gaertn., Lotus japonicus (Regel) K.Larsen and Phaseolus vulgaris L. One of the L. japonicus peptides, called LjCLE-RS2, has been structurally characterised and found to be an arabinosylated glycopeptide. All of the known nodulation CLE peptides act via an orthologous leucine rich repeat (LRR) receptor kinase. Perception of the peptide results in the production of a novel, unidentified inhibitor signal that acts to suppress further nodulation events. Here, we contrast and compare the various nodulation-suppressing CLE peptides of legumes.

scholarly journals Nitrate-Induced CLE Peptide Systemically Inhibits Nodulation in Medicago truncatula

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1456
Author(s):  
Maria Lebedeva ◽  
Mahboobeh Azarakhsh ◽  
Yaroslavna Yashenkova ◽  
Lyudmila Lutova
Keyword(s):  
Medicago Truncatula ◽  
Lotus Japonicus ◽  
Dependent Manner ◽  
Receptor Kinase ◽  
Nitrate Treatment ◽  
Whole Plant ◽  
Cle Peptides ◽  
Autoregulation Of Nodulation ◽  
Cle Peptide ◽  
Plant Level

Legume plants form nitrogen-fixing nodules in symbiosis with soil bacteria rhizobia. The number of symbiotic nodules is controlled at the whole-plant level with autoregulation of nodulation (AON), which includes a shoot-acting CLV1-like receptor kinase and mobile CLE (CLAVATA3/ENDOSPERM SURROUNDING REGION-related) peptides that are produced in the root in response to rhizobia inoculation. In addition to rhizobia-induced CLE peptides, nitrate-induced CLE genes have been identified in Lotus japonicus and Glycine max, which inhibited nodulation when overexpressed. However, nitrate-induced CLE genes that systemically suppress nodulation in AON-dependent manner have not been identified in Medicago truncatula. Here, we found that MtCLE35 expression is activated by both rhizobia inoculation and nitrate treatment in M. truncatula, similarly to L. japonicus CLE genes. Moreover, we found that MtCLE35 systemically suppresses nodulation in AON-dependent manner, suggesting that MtCLE35 may mediate nitrate-induced inhibition of nodulation in M. truncatula.

scholarly journals Characterisation of Medicago truncatula CLE34 and CLE35 in nodulation control

2020 ◽  
Author(s):  
Celine Mens ◽  
April H. Hastwell ◽  
Huanan Su ◽  
Peter M. Gresshoff ◽  
Ulrike Mathesius ◽  
...  
Keyword(s):  
Pisum Sativum ◽  
Medicago Truncatula ◽  
Sequence Homology ◽  
Dependent Manner ◽  
Legume Species ◽  
Mature Peptide ◽  
Cle Peptides ◽  
Autoregulation Of Nodulation ◽  
Cle Peptide ◽  
Distinct Role

AbstractLegume plants form a symbiosis with N2-fixing soil rhizobia, resulting in new root organs called nodules that enable N2-fixation. Nodulation is a costly process that is tightly regulated by the host through Autoregulation of Nodulation (AON) and nitrate-dependent regulation of nodulation. Both pathways require legume-specific CLAVATA/ESR-related (CLE) peptides. Nitrogen-induced nodulation-suppressing CLE peptides have not previously been characterised in Medicago truncatula, with only rhizobia-induced MtCLE12 and MtCLE13 identified. Here, we report on novel peptides MtCLE34 and MtCLE35 in nodulation control pathways. The nodulation-suppressing CLE peptides of five legume species were classified into three clades based on sequence homology and phylogeny. This approached identified MtCLE34 and MtCLE35 and four new CLE peptide orthologues of Pisum sativum. Whereas MtCLE12 and MtCLE13 are induced by rhizobia, MtCLE34 and MtCLE35 respond to both rhizobia and nitrate. MtCLE34 was identified as a pseudogene lacking a functional CLE-domain. Overexpression of MtCLE12, MtCLE13 and MtCLE35 inhibits nodulation. Together, our findings indicate that MtCLE12 and MtCLE13 have a distinct role in AON, while MtCLE35 regulates nodule numbers in a rhizobia- and nitrate-dependent manner. MtCLE34 likely had a similar role to MtCLE35 but its function was lost due to a nonsense mutation resulting in the loss of the mature peptide.

Identification of tissue-specific gene clusters and orthologues of nodulation-related genes in Vigna angularis

2014 ◽  
Vol 12 (S1) ◽  
pp. S21-S26 ◽  
Author(s):  
Yang Jae Kang ◽  
Jayern Lee ◽  
Yong Hwan Kim ◽  
Suk-Ha Lee
Keyword(s):  
De Novo ◽  
Transcriptome Assembly ◽  
Lotus Japonicus ◽  
Gene Clusters ◽  
Specific Gene ◽  
Vigna Angularis ◽  
Model Legume ◽  
Tissue Specific ◽  
Autoregulation Of Nodulation ◽  
Species Specific

Nitrogen fixation in legumes is an important agricultural trait that results from symbiosis between the root and rhizobia. To understand the molecular basis of nodulation, recent research has been focused on the identification of nodulation-related genes by functional analysis using two major model legumes, Medicago truncatula and Lotus japonicus. Thus far, three important processes have been discovered, namely Nod factor (NF) perception, NF signalling and autoregulation of nodulation. Nevertheless, application of the results of these studies is limited for non-model legume crops because a reference genome is unavailable. However, because the cost of whole-transcriptome analysis has dropped dramatically due to the Next generation sequencer (NGS) technology, minor crops for which reference sequences are yet to be constructed can still be studied at the genome level. In this study, we sequenced the leaf and root transcriptomes of Vigna angularis (accession IT213134) and de novo assembled. Our results demonstrate the feasibility of using the transcriptome assembly to effectively identify tissue-specific peptide clusters related to tissue-specific functions and species-specific nodulation-related genes.

scholarly journals Inoculation- and Nitrate-Induced CLE Peptides of Soybean Control NARK-Dependent Nodule Formation

2011 ◽  
Vol 24 (5) ◽  
pp. 606-618 ◽  
Author(s):  
Dugald E. Reid ◽  
Brett J. Ferguson ◽  
Peter M. Gresshoff
Keyword(s):  
Amino Acid ◽  
Nodule Development ◽  
Nodule Formation ◽  
Dependent Manner ◽  
Transgenic Roots ◽  
Nitrate Treatment ◽  
Cle Peptides ◽  
Autoregulation Of Nodulation ◽  
Cle Peptide ◽  
Bradyrhizobium Sp

Systemic autoregulation of nodulation in legumes involves a root-derived signal (Q) that is perceived by a CLAVATA1-like leucine-rich repeat receptor kinase (e.g. GmNARK). Perception of Q triggers the production of a shoot-derived inhibitor that prevents further nodule development. We have identified three candidate CLE peptide-encoding genes (GmRIC1, GmRIC2, and GmNIC1) in soybean (Glycine max) that respond to Bradyrhizobium japonicum inoculation or nitrate treatment. Ectopic overexpression of all three CLE peptide genes in transgenic roots inhibited nodulation in a GmNARK-dependent manner. The peptides share a high degree of amino acid similarity in a 12-amino-acid C-terminal domain, deemed to represent the functional ligand of GmNARK. GmRIC1 was expressed early (12 h) in response to Bradyrhizobium-sp.-produced nodulation factor while GmRIC2 was induced later (48 to 72 h) but was more persistent during later nodule development. Neither GmRIC1 nor GmRIC2 were induced by nitrate. In contrast, GmNIC1 was strongly induced by nitrate (2 mM) treatment but not by Bradyrhizobium sp. inoculation and, unlike the other two GmCLE peptides, functioned locally to inhibit nodulation. Grafting demonstrated a requirement for root GmNARK activity for nitrate regulation of nodulation whereas Bradyrhizobium sp.-induced regulation was contingent on GmNARK function in the shoot.

scholarly journals AP2 transcription factor CBX1 with a specific function in symbiotic exchange of nutrients in mycorrhizal Lotus japonicus

2018 ◽  
Vol 115 (39) ◽  
pp. E9239-E9246 ◽  
Author(s):  
Li Xue ◽  
Lompong Klinnawee ◽  
Yue Zhou ◽  
Georgios Saridis ◽  
Vinod Vijayakumar ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Dna Binding ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Phosphate Uptake ◽  
Lotus Japonicus ◽  
Binding Motif ◽  
Binding Studies ◽  
Am Symbiosis

The arbuscular mycorrhizal (AM) symbiosis, a widespread mutualistic association between land plants and fungi, depends on reciprocal exchange of phosphorus driven by proton-coupled phosphate uptake into host plants and carbon supplied to AM fungi by host-dependent sugar and lipid biosynthesis. The molecular mechanisms and cis-regulatory modules underlying the control of phosphate uptake and de novo fatty acid synthesis in AM symbiosis are poorly understood. Here, we show that the AP2 family transcription factor CTTC MOTIF-BINDING TRANSCRIPTION FACTOR1 (CBX1), a WRINKLED1 (WRI1) homolog, directly binds the evolutionary conserved CTTC motif that is enriched in mycorrhiza-regulated genes and activates Lotus japonicus phosphate transporter 4 (LjPT4) in vivo and in vitro. Moreover, the mycorrhiza-inducible gene encoding H+-ATPase (LjHA1), implicated in energizing nutrient uptake at the symbiotic interface across the periarbuscular membrane, is coregulated with LjPT4 by CBX1. Accordingly, CBX1-defective mutants show reduced mycorrhizal colonization. Furthermore, genome-wide–binding profiles, DNA-binding studies, and heterologous expression reveal additional binding of CBX1 to AW box, the consensus DNA-binding motif for WRI1, that is enriched in promoters of glycolysis and fatty acid biosynthesis genes. We show that CBX1 activates expression of lipid metabolic genes including glycerol-3-phosphate acyltransferase RAM2 implicated in acylglycerol biosynthesis. Our finding defines the role of CBX1 as a regulator of host genes involved in phosphate uptake and lipid synthesis through binding to the CTTC/AW molecular module, and supports a model underlying bidirectional exchange of phosphorus and carbon, a fundamental trait in the mutualistic AM symbiosis.

scholarly journals HP1 drives de novo 3D genome reorganization in early Drosophila embryos

Nature ◽  
2021 ◽  
Author(s):  
Fides Zenk ◽  
Yinxiu Zhan ◽  
Pavel Kos ◽  
Eva Löser ◽  
Nazerke Atinbayeva ◽  
...  
Keyword(s):  
Genome Organization ◽  
Molecular Mechanisms ◽  
High Throughput Sequencing ◽  
De Novo ◽  
Early Embryo ◽  
Heterochromatin Protein ◽  
Chromosome Conformation ◽  
3D Genome ◽  
Genome Reorganization

AbstractFundamental features of 3D genome organization are established de novo in the early embryo, including clustering of pericentromeric regions, the folding of chromosome arms and the segregation of chromosomes into active (A-) and inactive (B-) compartments. However, the molecular mechanisms that drive de novo organization remain unknown1,2. Here, by combining chromosome conformation capture (Hi-C), chromatin immunoprecipitation with high-throughput sequencing (ChIP–seq), 3D DNA fluorescence in situ hybridization (3D DNA FISH) and polymer simulations, we show that heterochromatin protein 1a (HP1a) is essential for de novo 3D genome organization during Drosophila early development. The binding of HP1a at pericentromeric heterochromatin is required to establish clustering of pericentromeric regions. Moreover, HP1a binding within chromosome arms is responsible for overall chromosome folding and has an important role in the formation of B-compartment regions. However, depletion of HP1a does not affect the A-compartment, which suggests that a different molecular mechanism segregates active chromosome regions. Our work identifies HP1a as an epigenetic regulator that is involved in establishing the global structure of the genome in the early embryo.

scholarly journals Copy number-dependent DNA methylation of the Pyricularia oryzae MAGGY retrotransposon is triggered by DNA damage

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Ba Van Vu ◽  
Quyet Nguyen ◽  
Yuki Kondo-Takeoka ◽  
Toshiki Murata ◽  
Naoki Kadotani ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Copy Number ◽  
Rna Silencing ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Pyricularia Oryzae ◽  
Transcriptional Gene Silencing ◽  
Physical Interaction ◽  
Uncharacterized Protein ◽  
Form Complex

AbstractTransposable elements are common targets for transcriptional and post-transcriptional gene silencing in eukaryotic genomes. However, the molecular mechanisms responsible for sensing such repeated sequences in the genome remain largely unknown. Here, we show that machinery of homologous recombination (HR) and RNA silencing play cooperative roles in copy number-dependent de novo DNA methylation of the retrotransposon MAGGY in the fungusPyricularia oryzae. Genetic and physical interaction studies revealed thatRecAdomain-containing proteins, includingP. oryzaehomologs ofRad51, Rad55, andRad57, together with an uncharacterized protein, Ddnm1, form complex(es) and mediate either the overall level or the copy number-dependence of de novo MAGGY DNA methylation, likely in conjunction with DNA repair. Interestingly,P. oryzaemutants of specific RNA silencing components (MoDCL1andMoAGO2)were impaired in copy number-dependence of MAGGY methylation. Co-immunoprecipitation of MoAGO2 and HR components suggested a physical interaction between the HR and RNA silencing machinery in the process.

scholarly journals The Prion-Like Spreading of Alpha-Synuclein in Parkinson’s Disease: Update on Models and Hypotheses

2021 ◽  
Vol 22 (15) ◽  
pp. 8338
Author(s):  
Asad Jan ◽  
Nádia Pereira Gonçalves ◽  
Christian Bjerggaard Vaegter ◽  
Poul Henning Jensen ◽  
Nelson Ferreira
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Alpha Synuclein ◽  
Experimental Models ◽  
Cellular Factors ◽  
Recent Developments ◽  
Novel Targets ◽  
Presynaptic Protein

The pathological aggregation of the presynaptic protein α-synuclein (α-syn) and propagation through synaptically coupled neuroanatomical tracts is increasingly thought to underlie the pathophysiological progression of Parkinson’s disease (PD) and related synucleinopathies. Although the precise molecular mechanisms responsible for the spreading of pathological α-syn accumulation in the CNS are not fully understood, growing evidence suggests that de novo α-syn misfolding and/or neuronal internalization of aggregated α-syn facilitates conformational templating of endogenous α-syn monomers in a mechanism reminiscent of prions. A refined understanding of the biochemical and cellular factors mediating the pathological neuron-to-neuron propagation of misfolded α-syn will potentially elucidate the etiology of PD and unravel novel targets for therapeutic intervention. Here, we discuss recent developments on the hypothesis regarding trans-synaptic propagation of α-syn pathology in the context of neuronal vulnerability and highlight the potential utility of novel experimental models of synucleinopathies.

scholarly journals Examination of the Transcriptional Response to LaMIR166a Overexpression in Larix kaempferi (Lamb.) Carr

Biology ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 576
Author(s):  
Yanru Fan ◽  
Wanfeng Li ◽  
Zhexin Li ◽  
Shaofei Dang ◽  
Suying Han ◽  
...  
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
De Novo ◽  
Pearson Correlation ◽  
Transcriptional Response ◽  
Correlation Coefficients ◽  
Embryonic Cell ◽  
Larix Kaempferi ◽  
Transgenic Cell

The study of somatic embryogenesis can provide insight into early plant development. We previously obtained LaMIR166a-overexpressing embryonic cell lines of Larix kaempferi (Lamb.) Carr. To further elucidate the molecular mechanisms associated with miR166 in this species, the transcriptional profiles of wild-type (WT) and three LaMIR166a-overexpressing transgenic cell lines were subjected to RNA sequencing using the Illumina NovaSeq 6000 system. In total, 203,256 unigenes were generated using Trinity de novo assembly, and 2467 differentially expressed genes were obtained by comparing transgenic and WT lines. In addition, we analyzed the cleaved degree of LaMIR166a target genes LaHDZ31–34 in different transgenic cell lines by detecting the expression pattern of LaHdZ31–34, and their cleaved degree in transgenic cell lines was higher than that in WT. The downstream genes of LaHDZ31–34 were identified using Pearson correlation coefficients. Yeast one-hybrid and dual-luciferase report assays revealed that the transcription factors LaHDZ31–34 could bind to the promoters of LaPAP, LaPP1, LaZFP5, and LaPHO1. This is the first report of gene expression changes caused by LaMIR166a overexpression in Japanese larch. These findings lay a foundation for future studies on the regulatory mechanism of miR166.

scholarly journals Palmitoylation of Sindbis Virus TF Protein Regulates Its Plasma Membrane Localization and Subsequent Incorporation into Virions

2016 ◽  
Vol 91 (3) ◽  
Author(s):  
Jolene Ramsey ◽  
Emily C. Renzi ◽  
Randy J. Arnold ◽  
Jonathan C. Trinidad ◽  
Suchetana Mukhopadhyay
Keyword(s):  
Plasma Membrane ◽  
Sindbis Virus ◽  
Molecular Mechanisms ◽  
Wild Type Virus ◽  
Membrane Localization ◽  
Clear Understanding ◽  
Wild Type ◽  
Plasma Membrane Localization ◽  
C Terminus ◽  
N Terminus

ABSTRACT Palmitoylation is a reversible, posttranslational modification that helps target proteins to cellular membranes. The alphavirus small membrane proteins 6K and TF have been reported to be palmitoylated and to positively regulate budding. 6K and TF are isoforms that are identical in their N termini but unique in their C termini due to a −1 ribosomal frameshift during translation. In this study, we used cysteine (Cys) mutants to test differential palmitoylation of the Sindbis virus 6K and TF proteins. We modularly mutated the five Cys residues in the identical N termini of 6K and TF, the four additional Cys residues in TF's unique C terminus, or all nine Cys residues in TF. Using these mutants, we determined that TF palmitoylation occurs primarily in the N terminus. In contrast, 6K is not palmitoylated, even on these shared residues. In the C-terminal Cys mutant, TF protein levels increase both in the cell and in the released virion compared to the wild type. In viruses with the N-terminal Cys residues mutated, TF is much less efficiently localized to the plasma membrane, and it is not incorporated into the virion. The three Cys mutants have minor defects in cell culture growth but a high incidence of abnormal particle morphologies compared to the wild-type virus as determined by transmission electron microscopy. We propose a model where the C terminus of TF modulates the palmitoylation of TF at the N terminus, and palmitoylated TF is preferentially trafficked to the plasma membrane for virus budding. IMPORTANCE Alphaviruses are a reemerging viral cause of arthritogenic disease. Recently, the small 6K and TF proteins of alphaviruses were shown to contribute to virulence in vivo. Nevertheless, a clear understanding of the molecular mechanisms by which either protein acts to promote virus infection is missing. The TF protein is a component of budded virions, and optimal levels of TF correlate positively with wild-type-like particle morphology. In this study, we show that the palmitoylation of TF regulates its localization to the plasma membrane, which is the site of alphavirus budding. Mutants in which TF is not palmitoylated display drastically reduced plasma membrane localization, which effectively prevents TF from participating in budding or being incorporated into virus particles. Investigation of the regulation of TF will aid current efforts in the alphavirus field searching for approaches to mitigate alphaviral disease in humans.

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