The concept that proteins and small RNAs can move to and function in distant body parts is well established. However, non-cell-autonomy of small RNA molecules raises the question: To what extent are protein-coding messenger RNAs (mRNAs) exchanged between tissues in plants? Here we report the comprehensive identification of 2,006 genes producing mobile RNAs in Arabidopsis thaliana. The analysis of variant ecotype transcripts that were present in heterografted plants allowed the identification of mRNAs moving between various organs under normal or nutrient-limiting conditions. Most of these mobile transcripts seem to follow the phloem-dependent allocation pathway transporting sugars from photosynthetic tissues to roots via the vasculature. Notably, a high number of transcripts also move in the opposite, root-to-shoot direction and are transported to specific tissues including flowers. Proteomic data on grafted plants indicate the presence of proteins from mobile RNAs, allowing the possibility that they may be translated at their destination site. The mobility of a high number of mRNAs suggests that a postulated tissue-specific gene expression profile might not be predictive for the actual plant body part in which a transcript exerts its function
Hyperdiverse forests occur in the lowland tropics, whereas the most species-rich shrublands are found in regions such as south-western Australia (kwongan) and South Africa (fynbos). Despite large differences, these ecosystems share an important characteristic: their soils are strongly weathered and phosphorus (P) is a key growth-limiting nutrient. Soil-borne pathogens are increasingly being recognized as drivers of plant diversity in lowland tropical rainforests, but have received little attention in species-rich shrublands. We suggest a trade-off in which the species most proficient at acquiring P have ephemeral roots that are particularly susceptible to soil-borne pathogens. This could equalize out the differences in competitive ability among co-occurring species in these ecosystems, thus contributing to coexistence. Moreover, effective protection against soil-borne pathogens by ectomycorrhizal (ECM) fungi might explain the occurrence of monodominant stands of ECM trees and shrubs amongst otherwise species-rich communities. We identify gaps in our knowledge which need to be filled in order to evaluate a possible link between P limitation, fine root traits, soil-borne pathogens and local plant species diversity. Such a link may help to explain how numerous plant species can coexist in hyperdiverse rainforests and shrublands, and, conversely, how monodominant stands can develop in these ecosystems.
Fine roots acquire essential soil resources and mediate biogeochemical cycling in terrestrial ecosystems. Estimates of carbon and nutrient allocation to build and maintain these structures remain uncertain because of the challenges of consistently measuring and interpreting fine-root systems. Traditionally, fine roots have been defined as all roots ≤ 2 mm in diameter, yet it is now recognized that this approach fails to capture the diversity of form and function observed among fine-root orders. Here, we demonstrate how order-based and functional classification frameworks improve our understanding of dynamic root processes in ecosystems dominated by perennial plants. In these frameworks, fine roots are either separated into individual root orders or functionally defined into a shorter-lived absorptive pool and a longer-lived transport fine-root pool. Using these frameworks, we estimate that fine-root production and turnover represent 22% of terrestrial net primary production globally – a c. 30% reduction from previous estimates assuming a single fine-root pool. Future work developing tools to rapidly differentiate functional fine-root classes, explicit incorporation of mycorrhizal fungi into fine-root studies, and wider adoption of a two-pool approach to model fine roots provide opportunities to better understand below-ground processes in the terrestrial biosphere.
Tyrosine phosphorylation is an important post-translational modification that is known to regulate receptor kinase (RK)-mediated signaling in animals. Plant RKs are annotated as serine/threonine kinases, but recent work has revealed that tyrosine phosphorylation is also crucial for the activation of RK-mediated signaling in plants. These initial observations have paved the way for subsequent detailed studies on the mechanism of activation of plant RKs and the biological relevance of tyrosine phosphorylation for plant growth and immunity. In this Opinion article we review recent reports on the contribution of RK tyrosine phosphorylation in plant growth and immunity; we propose that tyrosine phosphorylation plays a major regulatory role in the initiation and transduction of RK-mediated signaling in plants.
Using hundreds of samples of field-grown rice (Oryza sativa) leaves, we developed a statistical model for the expression of circadian clock-related genes integrating diurnally entrained circadian clock with phase setting by light, both responses to light and temperature gated by the circadian clock. We show that expression of individual genes was strongly affected by temperature. However, internal time estimated from expression of multiple genes, which may reflect transcriptional regulation of downstream genes, is punctual to 22 min and not affected by weather, daylength, or plant developmental age in the field. Thus, we demonstrated that the circadian clock is a regulatory network of multiple genes that retains accurate physical time of day by integrating the perturbations on individual genes under fluctuating environments in the field.
Type IV secretion systems (T4SSs) are multiprotein complexes that transport effector proteins and protein–DNA complexes through bacterial membranes to the extracellular milieu or directly into the cytoplasm of other cells. Many bacteria of the family Xanthomonadaceae, which occupy diverse environmental niches, carry a T4SS with unknown function but with several characteristics that distinguishes it from other T4SSs. Here we show that the Xanthomonas citri T4SS provides these cells the capacity to kill other Gram-negative bacterial species in a contact-dependent manner. The secretion of one type IV bacterial effector protein is shown to require a conserved C-terminal domain and its bacteriolytic activity is neutralized by a cognate immunity protein whose 3D structure is similar to peptidoglycan hydrolase inhibitors. This is the first demonstration of the involvement of a T4SS in bacterial killing and points to this special class of T4SS as a mediator of both antagonistic and cooperative interbacterial interactions.
Diorge P. Souza, Gabriel U. Oka, Cristina E. Alvarez-Martinez, Alexandre W. Bisson-Filho, German Dunger, Lise Hobeika, Nayara S. Cavalcante, Marcos C. Alegria, Leandro R.S. Barbosa, Roberto K. Salinas, Cristiane R. Guzzo & Chuck S. Farah
A cluster of three rice lectin receptor kinases confers resistance to planthopper insects.
Insect pests reduce yields of crops worldwide through direct damage and because they spread devastating viral diseases. In Asia, the brown planthopper (BPH) decimates rice (Oryza sativa) crops, causing the loss of billions of dollars annually1. In this issue, Liu et al.2 report the cloning of a rice genetic locus that confers broad-spectrum resistance to BPH and at least one other planthopper species (white back planthopper). Introducing this locus into plant genomes is likely to provide an effective means of combating insect pests of rice and of other cereals such as maize.
In modern rice agriculture, BPH damage is controlled through breeding and the application of vast amounts of chemical pesticides1. Pesticides are not a sustainable approach, however, owing to high costs, harmful environmental effects and rapid development of resistant insects. Breeding programs have identified more than 20 genetic loci in cultivated or wild rice species that confer BPH resistance1. However, these Bph loci are usually only effective against specific BPH biotypes, and newly evolved BPH populations have rapidly overcome several Bph resistance loci deployed in the field..
Of the >20 identified Bph loci, only Bph14 and Bph26 have been cloned. Both of these loci encode coiled-coil, nucleotide-binding and leucine-rich repeat proteins3, 4, the main class of plant intracellular immune receptors5. Bph3 is a resistance locus that was first pinpointed genetically in the Sri Lankan rice indica cultivar Rathu Heenati. Notably, unlike most other Bph loci, including Bph14 and Bph26, Bph3 confers broad-spectrum resistance to many BPH biotypes as well as to the white back planthopper1, 2. The success of Bph3 as a resistance locus might be linked to the fact that it acts against BPH at an early stage of the feeding cycle, before the insect can deploy its arsenal of virulence proteins that circumvent plant defenses.
Despite the huge potential of Bph3 for rice agriculture, its molecular identity has been unknown. Liu et al.2 now identify Bph3 through map-based cloning in a cross between the resistant indica cultivar Rathu Heenati and the susceptible japonica cultivar 02428. Bph3 maps to a 79-kb genomic region that contains a cluster of three lectin receptor kinases, OsLecRK1–3 (ref. 2) (Fig. 1). The authors find that single-nucleotide polymorphisms in these genes are associated with BPH resistance in different cultivated rice accessions. They also show that ectopic expression of the OsLecRK1–3 gene cluster in the susceptible japonica Kitaake cultivar confers BPH resistance.
The brown planthopper (BPH) is the most destructive pest of rice (Oryza sativa) and a substantial threat to rice production, causing losses of billions of dollars annually1, 2. Breeding of resistant cultivars is currently hampered by the rapid breakdown of BPH resistance2. Thus, there is an urgent need to identify…
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So not open-access that Nature Biotech doesn't even give you the full abstract.
Many animal and plant pathogenic bacteria inject type III effector (T3E) proteins into their eukaryotic host cells to suppress immunity. The YopJ-family of T3Es is a widely distributed family of effector proteins found in both, animal and plant pathogens and its members are highly diversified in virulence functions. Some members have been shown to possess acetyltransferase activity; however, whether this is a general feature of YopJ-family T3Es is currently unknown. The T3E XopJ, a YopJ-family effector from the plant pathogen Xanthomonas campestris pv. vesicatoria, interacts with the proteasomal subunit RPT6 in planta to suppress proteasome activity resulting in the inhibition of salicylic acid (SA)-related immune responses. Here we show that XopJ has protease activity to specifically degrade RPT6, leading to reduced proteasome activity in the cytoplasm as well as in the nucleus. Proteolytic degradation of RPT6 was dependent on localization of XopJ to the plasma membrane as well as on its catalytic triad. Mutation of the Walker-B motif of RPT6 prevented XopJ-mediated degradation of the protein but not XopJ interaction. This indicates that interaction of RPT6 with XopJ is dependent on ATP-binding activity of RPT6 but proteolytic cleavage additionally requires its ATPase activity. Inhibition of the proteasome impairs the proteasomal turnover of NPR1, the master regulator of SA responses, leading to the accumulation of ubiquitinated NPR1 which likely interferes with full induction of NPR1 target genes. Our results show that YopJ-family T3Es are not only highly diversified in virulence function, but also appear to possess different biochemical activities.
The domestication of starch crops underpinned the development of human civilisation, yet we still do not fully understand how plants make starch. Starch is composed of glucose polymers that are branched (amylopectin) or linear (amylose). The amount of amylose strongly influences the physico-chemical behaviour of starchy foods during cooking and of starch mixtures in non-food manufacturing processes. The GRANULE-BOUND STARCH SYNTHASE (GBSS) is the glucosyltransferase specifically responsible for elongating amylose polymers and was the only protein known to be required for its biosynthesis. Here, we demonstrate that PROTEIN TARGETING TO STARCH (PTST) is also specifically required for amylose synthesis in Arabidopsis. PTST is a plastidial protein possessing an N-terminal coiled coil domain and a C-terminal carbohydrate binding module (CBM). We discovered that Arabidopsis ptst mutants synthesise amylose-free starch and are phenotypically similar to mutants lacking GBSS. Analysis of granule-bound proteins showed a dramatic reduction of GBSS protein in ptst mutant starch granules. Pull-down assays with recombinant proteins in vitro, as well as immunoprecipitation assays in planta, revealed that GBSS physically interacts with PTST via a coiled coil. Furthermore, we show that the CBM domain of PTST, which mediates its interaction with starch granules, is also required for correct GBSS localisation. Fluorescently tagged Arabidopsis GBSS, expressed either in tobacco or Arabidopsis leaves, required the presence of Arabidopsis PTST to localise to starch granules. Mutation of the CBM of PTST caused GBSS to remain in the plastid stroma. PTST fulfils a previously unknown function in targeting GBSS to starch. This sheds new light on the importance of targeting biosynthetic enzymes to sub-cellular sites where their action is required. Importantly, PTST represents a promising new gene target for the biotechnological modification of starch composition, as it is exclusively involved in amylose synthesis.
Plant-infecting viruses are transmitted by a diverse array of organisms including insects, mites, nematodes, fungi, and plasmodiophorids. Virus interactions with these vectors are diverse, but there are some commonalities. Generally the infection cycle begins with the vector encountering the virus in the plant and the virus is acquired by the vector. The virus must then persist in or on the vector long enough for the virus to be transported to a new host and delivered into the plant cell. Plant viruses rely on their vectors for breaching the plant cell wall to be delivered directly into the cytosol. In most cases, viral capsid or membrane glycoproteins are the specific viral proteins that are required for transmission and determinants of vector specificity. Specific molecules in vectors also interact with the virus and while there are few-identified to no-identified receptors, candidate recognition molecules are being further explored in these systems. Due to the specificity of virus transmission by vectors, there are defined steps that represent good targets for interdiction strategies to disrupt the disease cycle. This review focuses on new technologies that aim to disrupt the virus–vector interaction and focuses on a few of the well-characterized virus–vector interactions in the field. In closing, we discuss the importance of integration of these technologies with current methods for plant virus disease control.
Most transgenic crops are produced through tissue culture. The impact of utilizing such methods on the plant epigenome is poorly understood. Here we generated whole-genome, single-nucleotide resolution maps of DNA methylation in several regenerated rice lines. We found that all tested regenerated plants had significant losses of methylation compared to non-regenerated plants. Loss of methylation was largely stable across generations, and certain sites in the genome were particularly susceptible to loss of methylation. Loss of methylation at promoters was associated with deregulated expression of protein-coding genes. Analyses of callus and untransformed plants regenerated from callus indicated that loss of methylation is stochastically induced at the tissue culture step. These changes in methylation may explain a component of somaclonal variation, a phenomenon in which plants derived from tissue culture manifest phenotypic variability.
MicroRNAs (miRNAs) are small regulatory RNA molecules that inhibit the expression of specific target genes by binding to and cleaving their messenger RNAs or otherwise inhibiting their translation into proteins1. miRNAs are transcribed as much larger primary transcripts (pri-miRNAs), the function of which is not fully understood. Here we show that plant pri-miRNAs contain short open reading frame sequences that encode regulatory peptides. The pri-miR171b ofMedicago truncatula and the pri-miR165a of Arabidopsis thaliana produce peptides, which we term miPEP171b and miPEP165a, respectively, that enhance the accumulation of their corresponding mature miRNAs, resulting in downregulation of target genes involved in root development. The mechanism of miRNA-encoded peptide (miPEP) action involves increasing transcription of the pri-miRNA. Five other pri-miRNAs of A. thaliana and M. truncatula encode active miPEPs, suggesting that miPEPs are widespread throughout the plant kingdom. Synthetic miPEP171b and miPEP165a peptides applied to plants specifically trigger the accumulation of miR171b and miR165a, leading to reduction of lateral root development and stimulation of main root growth, respectively, suggesting that miPEPs might have agronomical applications.
Perception of pathogen (or microbe)-associated molecular patterns (PAMPs/MAMPs) by pattern recognition receptors (PRRs) is a key component of plant innate immunity. The Arabidopsis PRR EF-Tu receptor (EFR) recognizes the bacterial PAMP elongation factor Tu (EF-Tu) and its derived peptide elf18. Previous work revealed that transgenic expression of AtEFR in Solanaceae confers elf18 responsiveness and broad-spectrum bacterial disease resistance. In this study, we developed a set of bioassays to study the activation of PAMP-triggered immunity (PTI) in wheat. We generated transgenic wheat (Triticum aestivum) plants expressing AtEFR driven by the constitutive rice actin promoter and tested their response to elf18. We show that transgenic expression of AtEFR in wheat confers recognition of elf18, as measured by the induction of immune marker genes and callose deposition. When challenged with the cereal bacterial pathogen Pseudomonas syringae pv. oryzae, transgenic EFR wheat lines had reduced lesion size and bacterial multiplication. These results demonstrate that AtEFR can be transferred successfully from dicot to monocot species, further revealing that immune signalling pathways are conserved across these distant phyla. As novel PRRs are identified, their transfer between plant families represents a useful strategy for enhancing resistance to pathogens in crops.
Increased plant productivity and decreased microbial respiratory C loss can potentially mitigate increasing atmospheric CO2, but we currently lack effective means to achieve these goals. Soil microbes may play critical roles in mediating plant productivity and soil C/N dynamics under future climate scenarios of elevated CO2 (eCO2) through optimizing functioning of the root-soil interface. By using a labeling technique with 13C and 15N, we examined the effects of plant growth-promoting Pseudomonas fluorescens on C and N cycling in the rhizosphere of a common grass species under eCO2. These microbial inoculants were shown to increase plant productivity. Although strong competition for N between the plant and soil microbes was observed, the plant can increase its capacity to store more biomass C per unit of N under P. fluorescens addition. Unlike eCO2 effects, P. fluorescens inoculants did not change mass-specific microbial respiration and accelerate soil decomposition related to N cycling, suggesting these microbial inoculants mitigated positive feedbacks of soil microbial decomposition to eCO2. The potential to mitigate climate change by optimizing soil microbial functioning by plant growth-promoting Pseudomonas fluorescens is a prospect for ecosystem management.
During the transition from water to land, plants had to cope with the loss of water through transpiration, the inevitable result of photosynthetic CO2 fixation on land [ 1, 2 ]. Control of transpiration became possible through the development of a new cell type: guard cells, which form stomata. In vascular plants, stomatal regulation is mediated by the stress hormone ABA, which triggers the opening of the SnR kinase OST1-activated anion channel SLAC1 [ 3, 4 ]. To understand the evolution of this regulatory circuit, we cloned both ABA-signaling elements, SLAC1 and OST1, from a charophyte alga, a liverwort, and a moss, and functionally analyzed the channel-kinase interactions. We were able to show that the emergence of stomata in the last common ancestor of mosses and vascular plants coincided with the origin of SLAC1-type channels capable of using the ancient ABA drought signaling kinase OST1 for regulation of stomatal closure.
MPMI has played a leading role in disseminating new insights into plant-microbe interactions and promoting new approaches. Articles in this Focus Issue highlight the power of genomic studies in uncovering novel determinants of plant interactions with microbial symbionts (good), pathogens (bad), and complex microbial communities (unknown). Many articles also illustrate how genomics can support translational research by quickly advancing our knowledge of important microbes that have not been widely studied.
Click on Next Article or Table of Contents above to view the articles in this Focus Issue. (From the mobile site, go to the MPMI March 2015 issue.)
The biotrophic fungus Ustilago maydis causes smut disease in maize with characteristic tumor formation and anthocyanin induction. Here, we show that anthocyanin biosynthesis is induced by the virulence promoting secreted effector protein Tin2. Tin2 protein functions inside plant cells where it interacts with maize protein kinase ZmTTK1. Tin2 masks a ubiquitin–proteasome degradation motif in ZmTTK1, thus stabilizing the active kinase. Active ZmTTK1 controls activation of genes in the anthocyanin biosynthesis pathway. Without Tin2, enhanced lignin biosynthesis is observed in infected tissue and vascular bundles show strong lignification. This is presumably limiting access of fungal hyphae to nutrients needed for massive proliferation. Consistent with this assertion, we observe that maize brown midrib mutants affected in lignin biosynthesis are hypersensitive to U. maydis infection. We speculate that Tin2 rewires metabolites into the anthocyanin pathway to lower their availability for other defense responses.
Author Summary Plant roots are programmed to grow continuously into the soil, searching for nutrients and water. The iterative process of cell division, elongation, and differentiation contributes to root growth. The quiescent center (QC) is known to maintain the root meristem, and thus ensure root growth. In this study, we report a novel aspect of root growth regulation controlled independently of the QC by PHABULOSA (PHB). In shr mutant plants, PHB, which in the meristem is actively restricted to the central region of the stele by SHORTROOT (SHR) via miR165/6 , suppresses root meristem activity leading to root growth arrest. A high concentration of PHB in the stele does this by modulating B-ARR activity through a QC-independent pathway. Accordingly, we observed a significant recovery of root meristem activity and growth in the shr phb double mutant, while the QC remained absent. However, the presence of QC may be required to sustain continuous root growth. On the basis of our results, we propose that SHR maintains root growth via two separate pathways: by modulating PHB levels in the root stele, and by maintaining the QC identity.
The modification of proteins by the attachment of fatty acids is a targeting tactic involved in mechanisms of both plant immunity and bacterial pathogenesis. The plant plasma membrane (PM) is a key battleground in the war against disease-causing microbes. This membrane is armed with an array of sensor proteins that function as a surveillance system to detect invading pathogens. Several of these sensor proteins are directed to the plasma membrane through the covalent addition of fatty acids, a process termed fatty acylation. Phytopathogens secrete effector proteins into the plant cell to subvert these surveillance mechanisms, rendering the host susceptible to infection. The targeting of effectors to specific locales within plant cells, particularly the internal face of the host PM, is critical for their virulence function. Several bacterial effectors hijack the host fatty acylation machinery to be modified and directed to this contested locale. To find and fight these fatty acylated effectors the plant leverages lipid-modified intracellular sensors. This review provides examples featuring how fatty acylation is a battle tactic used by both combatants in the molecular arms race between plants and pathogens. Also highlighted is the exploitation of a specific form of host-mediated fatty acid modification, which appears to be exclusively employed by phytopathogenic effector proteins.
The Genome Balance Hypothesis originated from a recent study that provided a mechanism for the phenomenon of genome dominance in ancient polyploids: unique 24nt RNA coverage near genes is greater in genes on the recessive subgenome irrespective of differences in gene expression. 24nt RNAs target transposons. Transposon position effects are now hypothesized to balance the expression of networked genes and provide spring-like tension between pericentromeric heterochromatin and microtubules. The balance (coordination) of gene expression and centromere movement are under selection. Our hypothesis states that this balance can be maintained by many or few transposons about equally well. We explain known, balanced distributions of junk DNA within genomes, and between subgenomes in allopolyploids (and our hypothesis passes “the onion test” for any so-called solution to the C-value paradox). Importantly, when the allotetraploid maize chromosomes delete redundant genes, their nearby transposons are also lost; this result is explained if transposons near genes function. The Genome Balance Hypothesis is hypothetical because the position effect mechanisms implicated are not proved to apply to all junk DNA, and the continuous nature of the centromeric and gene position effects have not yet been studied as a single phenomenon.
How generalist parasites with wide host ranges can evolve is a central question in parasite evolution. Albugo candida is an obligate biotrophic parasite that consists of many physiological races that each specialize on distinct Brassicaceae host species. By analyzing genome sequence assemblies of five isolates, we show they represent three races that are genetically diverged by ~1%. Despite this divergence, their genomes are mosaic-like, with ~25% being introgressed from other races. Sequential infection experiments show that infection by adapted races enables subsequent infection of hosts by normally non-infecting races. This facilitates introgression and the exchange of effector repertoires, and may enable the evolution of novel races that can undergo clonal population expansion on new hosts. We discuss recent studies on hybridization in other eukaryotes such as yeast, Heliconius butterflies, Darwin's finches, sunflowers and cichlid fishes, and the implications of introgression for pathogen evolution in an agro-ecological environment.
Plant disease resistance is often mediated by nucleotide binding-leucine rich repeat (NLR) proteins which remain auto-inhibited until recognition of specific pathogen-derived molecules causes their activation, triggering a rapid, localized cell death called a hypersensitive response (HR). Three domains are recognized in one of the major classes of NLR proteins: a coiled-coil (CC), a nucleotide binding (NB-ARC) and a leucine rich repeat (LRR) domains. The maize NLR gene Rp1-D21 derives from an intergenic recombination event between two NLR genes, Rp1-D and Rp1-dp2 and confers an autoactive HR. We report systematic structural and functional analyses of Rp1 proteins in maize and N. benthamiana to characterize the molecular mechanism of NLR activation/auto-inhibition. We derive a model comprising the following three main features: Rp1 proteins appear to self-associate to become competent for activity. The CC domain is signaling-competent and is sufficient to induce HR. This can be suppressed by the NB-ARC domain through direct interaction. In autoactive proteins, the interaction of the LRR domain with the NB-ARC domain causes de-repression and thus disrupts the inhibition of HR. Further, we identify specific amino acids and combinations thereof that are important for the auto-inhibition/activity of Rp1 proteins. We also provide evidence for the function of MHD2, a previously uncharacterized, though widely conserved NLR motif. This work reports several novel insights into the precise structural requirement for NLR function and informs efforts towards utilizing these proteins for engineering disease resistance.
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