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Plant pathogens like virus, bacteria, and fungi incur a huge loss of global productivity. Targeting the dominant R gene resulted in the evolution of resistance in pathogens, which shifted plant pathologists' attention toward host susceptibility factors (or S genes). Herein, the application of sequence-specific nucleases (SSNs) for targeted genome editing are gaining more importance, which utilize the use of meganucleases (MN), zinc finger nucleases (ZFNs), transcription activator-like effector-based nucleases (TALEN) with the latest one namely clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9). The first generation of genome editing technologies, due to their cumbersome nature, is becoming obsolete. Owing to its simple and inexpensive nature the use of CRISPR/Cas9 system has revolutionized targeted genome editing technology. CRISPR/Cas9 system has been exploited for developing resistance against virus, bacteria, and fungi. For resistance to DNA viruses (mainly single-stranded DNA viruses), different parts of the viral genome have been targeted transiently and by the development of transgenic plants. For RNA viruses, mainly the host susceptibility factors and very recently the viral RNA genome itself have been targeted. Fungal and bacterial resistance has been achieved mainly by targeting the host susceptibility genes through the development of transgenics. In spite of these successes CRISPR/Cas9 system suffers from off-targeting. This and other problems associated with this system are being tackled by the continuous discovery/evolution of new variants. Finally, the regulatory standpoint regarding CRISPR/Cas9 will determine the fate of using this versatile tool in developing pathogen resistance in crop plants.

The generation and maintenance of functional variation in the pathogen defense system of plants is central to the constant evolutionary battle between hosts and parasites. If a species is susceptible to a given pathogen, hybridization and subsequent introgression of a resistance allele from a related species can potentially be an important source of new immunity and is therefore expected to be selected for in a process referred to as adaptive introgression. Here, we survey sequence variation in 10 resistance (R-) genes and compare them with 37 reference genes in natural populations of the two closely related and interfertile species: Arabidopsis lyrata and A. halleri. The R-genes are highly polymorphic in both species and show clear signs of trans-species polymorphisms. We show that A. lyrata and A. halleri have had a history of limited introgression for the reference genes. For the R-genes, the introgression rate has been significantly higher than for the reference genes, resulting in fewer fixed differences between species and a higher sharing of identical haplotypes. We conclude that R-genes likely cross the species boundaries at a higher rate than reference genes and therefore also that some of the increased diversity and trans-specific polymorphisms in R-genes is due to adaptive introgression.

Abscisic acid (ABA) is a stress hormone that accumulates under different abiotic and biotic stresses. A typical effect of ABA on leaves is to reduce transpirational water loss by closing stomata and parallelly defend against microbes by restricting their entry through stomatal pores. ABA can also promote the accumulation of polyamines, sphingolipids, and even proline. Stomatal closure by compounds other than ABA also helps plant defense against both abiotic and biotic stress factors. Further, ABA can interact with other hormones, such as methyl jasmonate (MJ) and salicylic acid (SA). Such cross-talk can be an additional factor in plant adaptations against environmental stresses and microbial pathogens. The present review highlights the recent progress in understanding ABA’s multifaceted role under stress conditions, particularly stomatal closure. We point out the importance of reactive oxygen species (ROS), reactive carbonyl species (RCS), nitric oxide (NO), and Ca 2+ in guard cells as key signaling components during the ABA-mediated short-term plant defense reactions. The rise in ROS, RCS, NO, and intracellular Ca 2+ triggered by ABA can promote additional events involved in long-term adaptive measures, including gene expression, accumulation of compatible solutes to protect the cell, hypersensitive response (HR), and programmed cell death (PCD). Several pathogens can counteract and try to reopen stomata. Similarly, pathogens attempt to trigger PCD of host tissue to their benefit. Yet, ABA-induced effects independent of stomatal closure can delay the pathogen spread and infection within leaves. Stomatal closure and other ABA influences can be among the early steps of defense and a crucial component of plants’ innate immunity response. Stomatal guard cells are quite sensitive to environmental stress and are considered good model systems for signal transduction studies. Further research on the ABA-induced stomatal closure mechanism can help us design strategies for plant/crop adaptations to stress.

Understanding gene variations in people living under extreme conditions has the potential of curing diseases caused by exposure to heat, cold, fatty diets, hypoxia, and pathogens. One candidate gene associated with heat resistance is ACE1, encoding angiotensin-converting enzyme 1. Associations have also been made between cold resistance or fatty diets and polymorphisms of several genes, including ACTN3, encoding alpha-actinin-3, and CPTIA, encoding carnitine palmitoyltransferase 1A. A prominent role in resistance to hypoxia has been recognized for polymorphisms of EPAS1, encoding endothelial PAS domain protein 1, and EGLN1, encoding Egl-9 family hypoxia inducible factor 1. Variants conferring human resistance to pathogens include HBB, encoding hemoglobin subunit beta, and ACE2, encoding angiotensin-converting enzyme 2. Genetic knowledge concerning such diseases as malaria and conditions such as hypoxia should continue to promote advances in gene therapy.

Background Pathogen infections seriously affect host health, and the use of antibiotics increases the risk of the emergence of drug-resistant bacteria and also increases environmental and health safety risks. Probiotics have received much attention for their excellent ability to prevent pathogen infections. Particularly, explaining mechanism of action of probiotics against pathogen infections is important for more efficient and rational use of probiotics and the maintenance of host health. Results Here, we describe the impacts of probiotic on host resistance to pathogen infections. Our findings revealed that (I) the protective effect of oral supplementation with B. velezensis against Aeromonas hydrophila infection was dependent on gut microbiota, specially the anaerobic indigenous gut microbe Cetobacterium ; (II) Cetobacterium was a sensor of health, especially for fish infected with pathogenic bacteria; (III) the genome resolved the ability of Cetobacterium somerae CS2105-BJ to synthesize vitamin B 12 de novo, while in vivo and in vitro metabolism assays also showed the ability of Cetobacterium somerae CS2105-BJ to produce vitamin B 12 ; (IV) the addition of vitamin B 12 significantly altered the gut redox status and the gut microbiome structure and function, and then improved the stability of the gut microbial ecological network, and enhanced the gut barrier tight junctions to prevent the pathogen infection. Conclusion Collectively, this study found that the effect of probiotics in enhancing host resistance to pathogen infections depended on function of B 12 produced by an anaerobic indigenous gut microbe, Cetobacterium . Furthermore, as a gut microbial regulator, B 12 exhibited the ability to strengthen the interactions within gut microbiota and gut barrier tight junctions, thereby improving host resistance against pathogen infection. 9wW3zJp3HpFrGEQCmLVC3S Video Abstract

The serine protease inhibitors (SPIs) are widely distributed in living organisms like bacteria, fungi, plants, and humans. The main function of SPIs as protease enzymes is to regulate the proteolytic activity. In plants, most of the studies of SPIs have been focused on their physiological role. The initial studies carried out in plants showed that SPIs participate in the regulation of endogenous proteolytic processes, as the regulation of proteases in seeds. Besides, it was observed that SPIs also participate in the regulation of cell death during plant development and senescence. On the other hand, plant SPIs have an important role in plant defense against pests and phytopathogenic microorganisms. In the last 20 years, several transgenic plants over-expressing SPIs have been produced and tested in order to achieve the increase of the resistance against pathogenic insects. Finally, in molecular farming, SPIs have been employed to minimize the proteolysis of recombinant proteins expressed in plants. The present review discusses the potential biotechnological applications of plant SPIs in the agriculture field.

Summary Pectate lyase genes have been documented as excellent candidates for improvement of fruit firmness. However, implementation of pectate lyase in regulating fruit postharvest deterioration has not been fully explored. In this report, 22 individual pectate lyase genes in tomato were identified, and one pectate lyase gene SlPL (Solyc03g111690) showed dominant expression during fruit maturation. RNA interference of SlPL resulted in enhanced fruit firmness and changes in pericarp cells. More importantly, the SlPL‐RNAi fruit demonstrated greater antirotting and pathogen‐resisting ability. Compared to wild‐type, SlPL‐RNAi fruit had higher levels of cellulose and hemicellulose, whereas the level of water‐soluble pectin was lower. Consistent with this, the activities of peroxidase, superoxide dismutase and catalase were higher in SlPL‐RNAi fruit, and the malondialdehyde concentration was lower. RNA‐Seq results showed large amounts of differentially expressed genes involved in hormone signalling, cell wall modification, oxidative stress and pathogen resistance. Collectively, these data demonstrate that pectate lyase plays an important role in both fruit softening and pathogen resistance. This may advance knowledge of postharvest fruit preservation in tomato and other fleshy fruit.

• Wounding triggers de novo organogenesis, vascular reconnection and defense response but how wound stress evoke such a diverse array of physiological responses remains unknown. • We previously identified AP2/ERF transcription factors, WOUND INDUCED DEDIFFERENTIATION1 (WIND1) and its homologs, WIND2, WIND3 and WIND4, as key regulators of wound-induced cellular reprogramming in Arabidopsis. To understand how WIND transcription factors promote downstream events, we performed time-course transcriptome analyses after WIND1 induction. • We observed a significant overlap between WIND1-induced genes and genes implicated in cellular reprogramming, vascular formation and pathogen response. We demonstrated that WIND transcription factors induce several reprogramming genes to promote callus formation at wound sites. We, in addition, showed that WIND transcription factors promote tracheary element formation, vascular reconnection and resistance to Pseudomonas syringae pv. tomato DC3000. • These results indicate that WIND transcription factors function as key regulators of woundinduced responses by promoting dynamic transcriptional alterations. This study provides deeper mechanistic insights into how plants control multiple physiological responses after wounding.

During plant development, sugar export is determinant in multiple processes such as nectar production, pollen development and long-distance sucrose transport. The plant SWEET family of sugar transporters is a recently identified protein family of sugar uniporters. In rice, SWEET transporters are the target of extracellular bacteria, which have evolved sophisticated mechanisms to modify their expression and acquire sugars to sustain their growth. Here we report the characterization of the SWEET family of sugar transporters in Vitis vinifera. We identified 17 SWEET genes in the V. vinifera 40024 genome and show that they are differentially expressed in vegetative and reproductive organs. Inoculation with the biotrophic pathogens Erysiphe necator and Plasmopara viticola did not result in significant induction of VvSWEET gene expression. However, infection with the necrotroph Botrytis cinerea triggered a strong up-regulation of VvSWEET4 expression. Further characterization of VvSWEET4 revealed that it is a glucose transporter localized in the plasma membrane that is up-regulated by inducers of reactive oxygen species and virulence factors from necrotizing pathogens. Finally, Arabidopsis knockout mutants in the orthologous AtSWEET4 were found to be less susceptible to B. cinerea. We propose that stimulation of expression of a developmentally regulated glucose uniporter by reactive oxygen species production and extensive cell death after necrotrophic fungal infection could facilitate sugar acquisition from plant cells by the pathogen. Short statement: Sugar transporter VvSWEET4 is up-regulated by infection with necrotizing pathogens, necrosis-inducing proteins and inducers of reactive oxygen species, suggesting a role in sugar redistribution during pathogen-induced cell death.

• The genes required for host-specific pathogenicity in Fusarium oxysporum can be acquired through horizontal chromosome transfer (HCT). However, it is unknown if HCT commonly contributes to the diversification of pathotypes. • Using comparative genomics and pathogenicity phenotyping, we explored the role of HCT in the evolution of F. oxysporum f. sp. fragariae, the cause of Fusarium wilt of strawberry, with isolates from four continents. • We observed two distinct syndromes: one included chlorosis (‘yellows-fragariae’) and the other did not (‘wilt-fragariae’). All yellows-fragariae isolates carried a predicted pathogenicity chromosome, ‘chrY-frag’, that was horizontally transferred at least four times. chrY-frag was associated with virulence on specific cultivars and encoded predicted effectors that were highly upregulated during infection. chrY-frag was not present in wilt-fragariae; isolates causing this syndrome evolved pathogenicity independently. All origins of F. oxysporum f. sp. fragariae occurred outside of the host’s native range. • Our data support the conclusion that HCT is widespread in F. oxysporum, but pathogenicity can also evolve independently. The absence of chrY-frag in wilt-fragariae suggests that multiple, distinct pathogenicity chromosomes can confer the same host specificity. The wild progenitors of cultivated strawberry (Fragaria × ananassa) did not co-evolve with this pathogen, yet we discovered several sources of genetic resistance.