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<jats:title>SUMMARY</jats:title><jats:p>Sorghum anthracnose caused by the fungus <jats:italic>Colletotrichum sublineola</jats:italic> (<jats:italic>Cs</jats:italic>) is a damaging disease of the crop. Here, we describe the identification of <jats:italic>ANTHRACNOSE RESISTANCE GENES</jats:italic> (<jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic>) encoding canonical nucleotide‐binding leucine‐rich repeat (NLR) receptors. <jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic> are dominant resistance genes identified in the sorghum lines SAP135 and P9830, respectively, that show broad‐spectrum resistance to <jats:italic>Cs</jats:italic>. Independent genetic studies using populations generated by crossing SAP135 and P9830 with TAM428, fine mapping using molecular markers, comparative genomics and gene expression studies determined that <jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic> are resistance genes against <jats:italic>Cs</jats:italic> strains. Interestingly, <jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic> are both located within clusters of duplicate NLR genes at linked loci separated by ~1 Mb genomic region. SAP135 and P9830 each carry only one of the <jats:italic>ARG</jats:italic> genes while having the recessive allele at the second locus. Only two copies of the <jats:italic>ARG5</jats:italic> candidate genes were present in the resistant P9830 line while five non‐functional copies were identified in the susceptible line. The resistant parents and their recombinant inbred lines carrying either <jats:italic>ARG4</jats:italic> or <jats:italic>ARG5</jats:italic> are resistant to strains Csgl1 and Csgrg suggesting that these genes have overlapping specificities. The role of <jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic> in resistance was validated through sorghum lines carrying independent recessive alleles that show increased susceptibility. <jats:italic>ARG4</jats:italic> and <jats:italic>ARG5</jats:italic> are located within complex loci displaying interesting haplotype structures and copy number variation that may have resulted from duplication. Overall, the identification of anthracnose resistance genes with unique haplotype stucture provides a foundation for genetic studies and resistance breeding.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>Drought stress caused by global warming has resulted in significant tree mortality, driving the evolution of water conservation strategies in trees. Although phytohormones have been implicated in morphological adaptations to water deficits, the molecular mechanisms underlying these processes in woody plants remain unclear. Here, we report that overexpression of <jats:italic>PtoMYB142</jats:italic> in <jats:italic>Populus tomentosa</jats:italic> results in a dwarfism phenotype with reduced leaf cell size, vessel lumen area, and vessel density in the stem xylem, leading to significantly enhanced drought resistance. We found that PtoMYB142 modulates gibberellin catabolism in response to drought stress by binding directly to the promoter of <jats:italic>PtoGA2ox4</jats:italic>, a GA<jats:sub>2</jats:sub>‐oxidase gene induced under drought stress. Conversely, knockout of <jats:italic>PtoMYB142</jats:italic> by the CRISPR/Cas9 system reduced drought resistance. Our results show that the reduced leaf size and vessel area, as well as the increased vessel density, improve leaf relative water content and stem water potential under drought stress. Furthermore, exogenous GA<jats:sub>3</jats:sub> application rescued GA‐deficient phenotypes in <jats:italic>PtoMYB142</jats:italic>‐overexpressing plants and reversed their drought resistance. By suppressing the expression of <jats:italic>PtoGA2ox4</jats:italic>, the manifestation of GA‐deficient characteristics, as well as the conferred resistance to drought in <jats:italic>PtoMYB142</jats:italic>‐overexpressing poplars, was impeded. Our study provides insights into the molecular mechanisms underlying tree drought resistance, potentially offering novel transgenic strategies to enhance tree resistance to drought.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>Previously, it has been shown that mutagenesis frequencies can be improved by directly fusing the human exonuclease TREX2 to Cas9, resulting in a strong increase in the frequency of smaller deletions at the cut site. Here, we demonstrate that, by using the SunTag system for recruitment of TREX2, the mutagenesis efficiency can be doubled in comparison to the direct fusion in <jats:italic>Arabidopsis thaliana</jats:italic>. Therefore, we also tested the efficiency of the system for targeted deletion formation by recruiting two other 3′‐5′ exonucleases, namely the human TREX1 and <jats:italic>E. coli</jats:italic> ExoI. It turns out that SunTag‐mediated recruitment of TREX1 not only improved the general mutation induction efficiency slightly in comparison to TREX2, but that, more importantly, the mean size of the induced deletions was also enhanced, mainly via an increase of deletions of 25 bp or more. EcExoI also yielded a higher amount of larger deletions. However, only in the case of TREX1 and TREX2, the effect was predominately SunTag‐dependent, indicating efficient target‐specific recruitment. Using SunTag‐mediated TREX1 recruitment at other genomic sites, we were able to obtain similar deletion patterns. Thus, we were able to develop an attractive novel editing tool that is especially useful for obtaining deletions in the range from 20 to 40 bp around the cut site. Such sizes are often required for the manipulation of cis‐regulatory elements. This feature is closing an existing gap as previous approaches, based on single nucleases or paired nickases or nucleases, resulted in either shorter or longer deletions, respectively.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>The yield of maize (<jats:italic>Zea mays</jats:italic> L.) crops depends on their ability to intercept sunlight throughout the growing cycle, transform this energy into biomass and allocate it to the kernels. Abiotic stresses affect these eco‐physiological determinants, reducing crop grain yield below the potential of each environment. Here we analyse the impact of combined abiotic stresses, such as water restriction and nitrogen deficiency or water restriction and elevated temperatures. Crop yield depends on the product of kernel yield per plant and the number of plants per unit soil area, but increasing plant population density imposes a crowding stress that reduces yield per plant, even within the range that maximises crop yield per unit soil area. Therefore, we also analyse the impact of abiotic stresses under different plant densities. We show that the magnitude of the detrimental effects of two combined stresses on field‐grown plants can be lower, similar or higher than the sum of the individual stresses. These patterns depend on the timing and intensity of each one of the combined stresses and on the effects of one of the stresses on the status of the resource whose limitation causes the other. The analysis of the eco‐physiological determinants of crop yield is useful to guide and prioritise the rapidly progressing studies aimed at understanding the molecular mechanisms underlying plant responses to combined stresses.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>Necrotrophic fungal plant pathogens employ cell death‐inducing proteins (CDIPs) to facilitate infection. However, the specific CDIPs and their mechanisms in pathogenic processes of <jats:italic>Sclerotinia sclerotiorum</jats:italic>, a necrotrophic pathogen that causes disease in many economically important crop species, have not yet been clearly defined. This study found that <jats:italic>S. sclerotiorum</jats:italic> secretes SsXyl2, a glycosyl hydrolase family 11 xylanase, at the late stage of hyphal infection. SsXyl2 targets the apoplast of host plants to induce cell death independent of xylanase activity. Targeted disruption of <jats:italic>SsXyl2</jats:italic> leads to serious impairment of virulence, which can be recovered by a catalytically impaired SsXyl2 variant, thus supporting the critical role of cell death‐inducing activity of SsXyl2 in establishing successful colonization of <jats:italic>S. sclerotiorum</jats:italic>. Remarkably, infection by <jats:italic>S. sclerotiorum</jats:italic> induces the accumulation of <jats:italic>Nicotiana benthamiana</jats:italic> hypersensitive‐induced reaction protein 2 (NbHIR2). NbHIR2 interacts with SsXyl2 at the plasma membrane and promotes its localization to the cell membrane and cell death‐inducing activity. Furthermore, gene‐edited mutants of <jats:italic>NbHIR2</jats:italic> displayed increased resistance to the wild‐type strain of <jats:italic>S. sclerotiorum</jats:italic>, but not to the <jats:italic>SsXyl2</jats:italic>‐deletion strain. Hence, SsXyl2 acts as a CDIP that manipulates host cell physiology by interacting with hypersensitive induced reaction protein to facilitate colonization by <jats:italic>S. sclerotiorum</jats:italic>. These findings provide valuable insights into the pathogenic mechanisms of CDIPs in necrotrophic pathogens and lead to a more promising approach for breeding resistant crops against <jats:italic>S. sclerotiorum</jats:italic>.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>Stalk lodging is a severe problem that limits maize production worldwide, although little attention has been given to its genetic basis. Here we measured rind penetrometer resistance (RPR), an effective index for stalk lodging, in a multi‐parent population of 1948 recombinant inbred lines (RILs) and an association population of 508 inbred lines (AMP508). Linkage and association mapping identified 53 and 29 single quantitative trait loci (QTLs) and 50 and 19 pairs of epistatic interactions for RPR in the multi‐parent population and AMP508 population, respectively. Phenotypic variation explained by all identified epistatic QTLs (up to ~5%) was much less than that explained by all single additive QTLs (up to ~33% in the multi‐parent population and ~ 60% in the AMP508 population). Among all detected QTLs, only eight single QTLs explained &gt;10% of phenotypic variation in single RIL populations. Alleles that increased RPR were enriched in tropical/subtropical (TST) groups from the AMP508 population. Based on genome‐wide association studies in both populations, we identified 137 candidate genes affecting RPR, which were assigned to multiple biological processes, such as the biosynthesis of cell wall components. Sixty‐six candidate genes were cross‐validated by multiple methods or populations. Most importantly, 23 candidate genes were upregulated or downregulated in high‐RPR lines relative to low‐RPR lines, supporting the associations between candidate genes and RPR. These findings reveal the complex nature of the genetic basis underlying RPR and provide loci or candidate genes for developing elite varieties that are resistant to stalk lodging via molecular breeding.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>As in many other organisms, tRNA‐derived RNAs (tDRs) exist in plants and likely have multiple functions. We previously showed that tDRs are present in Arabidopsis under normal growth conditions, and that the ones originating from alanine tRNAs are the most abundant in leaves. We also showed that tDRs Ala of 20 nt produced from mature tRNA<jats:sup>Ala</jats:sup> (AGC) can block in vitro protein translation. Here, we report that first, these tDRs Ala (AGC) can be found within peculiar foci in the cell that are neither P‐bodies nor stress granules and, second, that they assemble into intermolecular RNA G‐quadruplex (rG4) structures. Such tDR Ala rG4 structures can specifically interact with an Arabidopsis DEA(D/H) RNA helicase, the DExH1 protein, and unwind them. The rG4‐DExH1 protein interaction relies on a glycine‐arginine domain with RGG/RG/GR/GRR motifs present at the N‐terminal extremity of the protein. Mutations on the four guanine residues located at the 5′ extremity of the tDR Ala abolish its rG4 structure assembly, association with the DExH1 protein, and foci formation, but they do not prevent protein translation inhibition in vitro. Our data suggest that the sequestration of tDRs Ala into rG4 complexes might represent a way to modulate accessible and functional tDRs for translation inhibition within the plant cell <jats:italic>via</jats:italic> the activity of a specific RNA helicase, DExH1.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p><jats:italic>Actinidia</jats:italic> (‘<jats:italic>Mihoutao</jats:italic>’ in Chinese) includes species with complex ploidy, among which diploid <jats:italic>Actinidia chinensis</jats:italic> and hexaploid <jats:italic>Actinidia deliciosa</jats:italic> are economically and nutritionally important fruit crops. <jats:italic>Actinidia deliciosa</jats:italic> has been proposed to be an autohexaploid (2<jats:italic>n</jats:italic> = 174) with diploid <jats:italic>A. chinensis</jats:italic> (2<jats:italic>n</jats:italic> = 58) as the putative parent. A CCS‐based assembly anchored to a high‐resolution linkage map provided a chromosome‐resolved genome for hexaploid <jats:italic>A. deliciosa</jats:italic> yielded a 3.91‐Gb assembly of 174 pseudochromosomes comprising 29 homologous groups with 6 members each, which contain 39 854 genes with an average of 4.57 alleles per gene. Here we provide evidence that much of the hexaploid genome matches diploid <jats:italic>A. chinensis</jats:italic>; 95.5% of homologous gene pairs exhibited &gt;90% similarity. However, intragenome and intergenome comparisons of synteny indicate chromosomal changes. Our data, therefore, indicate that if <jats:italic>A. deliciosa</jats:italic> is an autoploid, chromosomal rearrangement occurred following autohexaploidy. A highly diversified pattern of gene expression and a history of rapid population expansion after polyploidisation likely facilitated the adaptation and niche differentiation of <jats:italic>A. deliciosa</jats:italic> in nature. The allele‐defined hexaploid genome of <jats:italic>A. deliciosa</jats:italic> provides new genomic resources to accelerate crop improvement and to understand polyploid genome evolution.</jats:p>

<jats:title>SUMMARY</jats:title><jats:p>Seed vigor has major impact on the rate and uniformity of seedling growth, crop yield, and quality. However, the epigenetic regulatory mechanism of crop seed vigor remains unclear. In this study, a (jumonji C) JmjC gene of the histone lysine demethylase <jats:italic>OsJMJ718</jats:italic> was cloned in rice, and its roles in seed germination and its epigenetic regulation mechanism were investigated. OsJMJ718 was located in the nucleus and was engaged in H3K9 methylation. Histochemical GUS staining analysis revealed OsJMJ718 was highly expressed in seed embryos. Abiotic stress strongly induced the <jats:italic>OsJMJ718</jats:italic> transcriptional accumulation level. Germination percentage and seedling vigor index of <jats:italic>OsJMJ718</jats:italic> knockout lines (<jats:italic>OsJMJ718</jats:italic>‐CR) were lower than those of the wild type (WT). Chromatin immunoprecipitation followed by sequencing (ChIP‐seq) of seeds imbibed for 24 h showed an increase in H3K9me3 deposition of thousands of genes in <jats:italic>OsJMJ718</jats:italic>‐CR. ChIP‐seq results and transcriptome analysis showed that differentially expressed genes were enriched in ABA and ethylene signal transduction pathways. The content of ABA in <jats:italic>OsJMJ718</jats:italic>‐CR was higher than that in WT seeds. <jats:italic>OsJMJ718</jats:italic> overexpression enhanced sensitivity to ABA during germination and early seedling growth. In the seed imbibition stage, ABA and ethylene content diminished and augmented, separately, suggesting that <jats:italic>OsJMJ718</jats:italic> may adjust rice seed germination through the ABA and ethylene signal transduction pathways. This study displayed the important function of <jats:italic>OsJMJ718</jats:italic> in adjusting rice seed germination and vigor, which will provide an essential reference for practical issues, such as improving rice vigor and promoting direct rice sowing production.</jats:p>