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With the emergence of high-throughput methods in plant biology, the importance of long-term projects characterized by incremental advances involving multiple laboratories can sometimes be overlooked. Here, I highlight my 40-year effort to isolate and characterize the most common class of mutants encountered in Arabidopsis (Arabidopsis thaliana): those defective in embryo development. I present an updated dataset of 510 EMBRYO-DEFECTIVE (EMB) genes identified throughout the Arabidopsis community; include important details on 2200 emb mutants and 241 pigment-defective embryo (pde) mutants analyzed in my laboratory; provide curated datasets with key features and publication links for each EMB gene identified; revisit past estimates of 500–1000 total EMB genes in Arabidopsis; document 83 double mutant combinations reported to disrupt embryo development; emphasize the importance of following established nomenclature guidelines and acknowledging allele history in research publications; and consider how best to extend community-based curation and screening efforts to approach saturation for this diverse class of mutants in the future. Continued advances in identifying EMB genes and characterizing their loss-of-function mutant alleles are needed to understand genotype-to-phenotype relationships in Arabidopsis on a broad scale, and to document the contributions of large numbers of essential genes to plant growth and development.

We studied the effects of two arbuscular mycorrhizal (AM) fungi, singly or together, on the outcome of competition between a host (tomato cultivar, wild-type (WT)) and a surrogate nonhost (rmc, a mycorrhiza-defective mutant of WT) as influenced by the contributions of the direct and AM phosphorus (P) uptake pathways to plant P. We grew plants singly or in pairs of the same or different genotypes (inoculated or not) in pots containing a small compartment with ³²P-labelled soil accessible to AM fungal hyphae and determined expression of orthophosphate (Pi) transporter genes involved in both AM and direct P uptake. Gigaspora margarita increased WT competitive effects on rmc. WT and rmc inoculated with Glomus intraradices both showed growth depressions, which were mitigated when G. margarita was present. Orthophosphate transporter gene expression and ³²P transfer showed that the AM pathway operated in single inoculated WT, but not in rmc. Effects of AM fungi on plant competition depended on the relative contributions of AM and direct pathways of P uptake. Glomus intraradices reduced the efficiency of direct uptake in both WT and rmc. The two-fungus combination showed that interactions between fungi are important in determining outcomes of plant competition.

RNA-directed DNA methylation (RdDM) is a biological process in which non-coding RNA molecules direct the addition of DNA methylation to specific DNA sequences. The RdDM pathway is unique to plants, although other mechanisms of RNA-directed chromatin modification have also been described in fungi and animals. To date, the RdDM pathway is best characterized within angiosperms (flowering plants), and particularly within the model plant Arabidopsis thaliana. However, conserved RdDM pathway components and associated small RNAs (sRNAs) have also been found in other groups of plants, such as gymnosperms and ferns. The RdDM pathway closely resembles other sRNA pathways, particularly the highly conserved RNAi pathway found in fungi, plants, and animals. Both the RdDM and RNAi pathways produce sRNAs and involve conserved Argonaute, Dicer and RNA-dependent RNA polymerase proteins. RdDM has been implicated in a number of regulatory processes in plants. The DNA methylation added by RdDM is generally associated with transcriptional repression of the genetic sequences targeted by the pathway. Since DNA methylation patterns in plants are heritable, these changes can often be stably transmitted to progeny. As a result, one prominent role of RdDM is the stable, transgenerational suppression of transposable element (TE) activity. RdDM has also been linked to pathogen defense, abiotic stress responses, and the regulation of several key developmental transitions. Although the RdDM pathway has a number of important functions, RdDM-defective mutants in Arabidopsis thaliana are viable and can reproduce, which has enabled detailed genetic studies of the pathway. However, RdDM mutants can have a range of defects in different plant species, including lethality, altered reproductive phenotypes, TE upregulation and genome instability, and increased pathogen sensitivity. Overall, RdDM is an important pathway in plants that regulates a number of processes by establishing and reinforcing specific DNA methylation patterns, which can lead to transgenerational epigenetic effects on gene expression and phenotype.

The rhizosheath, or the layer of soil closely adhering to roots, can help plants to tolerate drought under moderate soil drying conditions. Rhizosheath formation is the result of poorly understood interactions between root exudates, microbes, and soil conditions. Here, we study the roles played by the soil microbiota in rhizosheath formation in barley (a dry crop). We show that barley rhizosheath formation is greater in acid soil than in alkaline soil, and inoculation with microbiota from acid soil enhances rhizosheath formation in alkaline soil. The rhizosheath-promoting activity is associated with the presence of Flavobacteriaceae and Paenibacillaceae bacteria that express genes for biosynthesis of indole-3-acetic acid (IAA, a common auxin), as determined by metagenomics and metatranscriptomics. Two bacterial strains isolated from rhizosheath ( Chryseobacterium culicis and Paenibacillus polymyxa ) produce IAA and enhance barley rhizosheath formation, while their IAA-defective mutants are unable to promote rhizosheath formation. Co-inoculation with the IAA-producing strains enhances barley grain yield in field experiments through an increase in spike number. Our findings contribute to our understanding of barley rhizosheath formation, and suggest potential strategies for crop improvement. The rhizosheath, or the soil layer closely attached to roots, can help plants tolerate drought. Here, the authors show that rhizosheath formation in barley is promoted by soil bacteria that produce indole-3-acetic acid, a common auxin.

Angiogenesis contributes fundamentally to embryonic development, tissue homeostasis, and wound healing. Basic fibroblast growth factor (FGF2) is recognized as the first proangiogenic molecule discovered, and it facilitates angiogenesis by activating FGF receptor 1 (FGFR1) signaling in endothelial cells. However, the precise roles of FGFR and the FGF/FGFR signaling axis in angiogenesis remain unclear, especially because of the contradictory phenotypes of in vivo FGF and FGFR gene deficiency models. Our previous study results suggested a potential role of posttranslational small ubiquitin-like modifier modification (SUMOylation), with highly dynamic regulatory features, in vascular development and disorder. Here, we identified SENP1-regulated endothelial FGFR1 SUMOylation at conserved lysines responding to proangiogenic stimuli, while SENP1 functioned as the deSUMOylase. Hypoxia-enhanced FGFR1 SUMOylation restricted the tyrosine kinase activation of FGFR1 by modulating the dimerization of FGFR1 and FGFR1 binding with its phosphatase PTPRG. Consequently, it facilitated the recruitment of FRS2α to VEGFR2 but limited additional recruitment of FRS2α to FGFR1, supporting the activation of VEGFA/VEGFR2 signaling in endothelial cells. Furthermore, SUMOylation-defective mutation of FGFR1 resulted in exaggerated FGF2/FGFR1 signaling but suppressed VEGFA/VEGFR2 signaling and the angiogenic capabilities of endothelial cells, which were rescued by FRS2α overexpression. Reduced angiogenesis and endothelial sprouting in mice bearing an endothelial-specific, FGFR1 SUMOylation-defective mutant confirmed the functional significance of endothelial FGFR1 SUMOylation in vivo. Our findings identify the reversible SUMOylation of FGFR1 as an intrinsic fine-tuned mechanism in coordinating endothelial angiogenic signaling during neovascularization; SENP1-regulated FGFR1 SUMOylation and deSUMOylation controls the competitive recruitment of FRS2α by FGFR1 and VEGFR2 to switch receptor-complex formation responding to hypoxia and normoxia angiogenic environments.

Many chromatin-binding proteins and protein complexes that regulate transcription also bind RNA. One of these, Polycomb repressive complex 2 (PRC2), deposits the H3K27me3 mark of facultative heterochromatin and is required for stem cell differentiation. PRC2 binds RNAs broadly in vivo and in vitro. Yet, the biological importance of this RNA binding remains unsettled. Here, we tackle this question in human induced pluripotent stem cells by using multiple complementary approaches. Perturbation of RNA–PRC2 interaction by RNase A, by a chemical inhibitor of transcription or by an RNA-binding-defective mutant all disrupted PRC2 chromatin occupancy and localization genome wide. The physiological relevance of PRC2–RNA interactions is further underscored by a cardiomyocyte differentiation defect upon genetic disruption. We conclude that PRC2 requires RNA binding for chromatin localization in human pluripotent stem cells and in turn for defining cellular state. Perturbation of RNA–PRC2 interaction in human pluripotent stem cells disrupts PRC2 chromatin occupancy and localization genome wide. PRC2–RNA interactions contribute to cardiomyocyte differentiation.

This article is a Commentary on Meinke, 226: 306–325.

Arbuscular mycorrhizal fungi (AMF) can symbiose with many plants and improve nutrient uptake for their host plant. Rhizosphere microorganisms have been pointed to play important roles in helping AMF to mobilize soil insoluble nutrients, especially phosphorus. Whether the change in phosphate transport under AMF colonization will affect rhizosphere microorganisms is still unknown. Here, we evaluated the links of interactions among AMF and the rhizosphere bacterial community of maize ( Zea mays L.) by using a maize mycorrhizal defective mutant. Loss of mycorrhizal symbiosis function reduced the phosphorus concentration, biomass, and shoot length of maize colonized by AMF. Using 16S rRNA gene amplicon high-throughput sequencing, we found that the mutant material shifted the bacterial community in the rhizosphere under AMF colonization. Further functional prediction based on amplicon sequencing indicated that rhizosphere bacteria involved in sulfur reduction were recruited by the AMF colonized mutant but reduced in the AMF- colonized wild type. These bacteria harbored much abundance of sulfur metabolism-related genes and negatively correlated with biomass and phosphorus concentrations of maize. Collectively, this study shows that AMF symbiosis recruited rhizosphere bacterial communities to improve soil phosphate mobilization, which may also play a potential role in regulating sulfur uptake. This study provides a theoretical basis for improving crop adaptation to nutrient deficiency through soil microbial management practices.

Key messageThis study describes biological functions of the bHLH transcription factor RERJ1 involved in the jasmonate response and the related defense-associated metabolic pathways in rice, with particular focus on deciphering the regulatory mechanisms underlying stress-induced volatile emission and herbivory resistance. RERJ1 is rapidly and drastically induced by wounding and jasmonate treatment but its biological function remains unknown as yet. Here we provide evidence of the biological function of RERJ1 in plant defense, specifically in response to herbivory and pathogen attack, and offer insights into the RERJ1-mediated regulation of metabolic pathways of specialized defense compounds, such as monoterpene linalool, in possible collaboration with OsMYC2—a well-known master regulator in jasmonate signaling.In rice (Oryza sativa L.), the basic helix–loop–helix (bHLH) family transcription factor RERJ1 is induced under environmental stresses, such as wounding and drought, which are closely linked to jasmonate (JA) accumulation. Here, we investigated the biological function of RERJ1 in response to biotic stresses, such as herbivory and pathogen infection, using an RERJ1-defective mutant. Transcriptome analysis of the rerj1-Tos17 mutant revealed that RERJ1 regulated the expression of a typical family of conserved JA-responsive genes (e.g., terpene synthases, proteinase inhibitors, and jasmonate ZIM domain proteins). Upon exposure to armyworm attack, the rerj1-Tos17 mutant exhibited more severe damage than the wildtype, and significant weight gain of the larvae fed on the mutant was observed. Upon Xanthomonas oryzae infection, the rerj1-Tos17 mutant developed more severe symptoms than the wildtype. Among RERJ1-regulated terpene synthases, linalool synthase expression was markedly disrupted and linalool emission after wounding was significantly decreased in the rerj1-Tos17 mutant. RERJ1 appears to interact with OsMYC2—a master regulator of JA signaling—and many OsJAZ proteins, although no obvious epistatic interaction was detected between them at the transcriptional level. These results indicate that RERJ1 is involved in the transcriptional induction of JA-mediated stress-responsive genes via physical association with OsMYC2 and mediates defense against herbivory and bacterial infection through JA signaling.

The phenomenon of plant root tips sensing moisture gradient in soil and growing towards higher water potential is designated as root hydrotropism, which is critical for plants to survive when water is a limited factor. Molecular mechanisms regulating such a fundamental process, however, are largely unknown. Here we report our identification that cytokinins are key signaling molecules directing root growth orientation in a hydrostimulation (moisture gradient) condition. Lower water potential side of the root tip shows more cytokinin response relative to the higher water potential side. Consequently, two cytokinin downstream type-A response regulators, ARR16 and ARR17, were found to be up-regulated at the lower water potential side, causing increased cell division in the meristem zone, which allows the root to bend towards higher water potential side. Genetic analyses indicated that various cytokinin biosynthesis and signaling mutants, including the arr16 arr17 double mutant, are significantly less responsive to hydrostimulation. Consistently, treatments with chemical inhibitors interfering with either cytokinin biosynthesis or cell division completely abolished root hydrotropic response. Asymmetrically induced expression of ARR16 or ARR17 effectively led to root bending in both wild-type and miz1, a previously known hydrotropism-defective mutant. These data demonstrate that asymmetric cytokinin distribution is a primary determinant governing root hydrotropism.