A fundamental process culminating in the mechanisms of plant-pathogen interactions is the regulation of trophic divergence into biotrophic, hemibiotrophic, and necrotrophic interactions. Plant hormones, of almost all types, play significant roles in this regulatory apparatus. In plant-pathogen interactions, two classical mechanisms underlying hormone-dependent trophic divergence are long recognized. While salicylic acid dominates in the execution of host defense response against biotrophic and early-stage hemibiotrophic pathogens, jasmonic acid, and ethylene are key players facilitating host defense response against necrotrophic and later-stage hemibiotrophic pathogens. Evidence increasingly suggests that trophic divergence appears to be modulated by more complex signaling networks. Acting antagonistically or agonistically, other hormones such as auxins, cytokinins, abscisic acid, gibberellins, brassinosteroids, and strigolactones, as well as nitric oxide, are emerging candidates in the regulation of trophic divergence. In this review, the latest advances in the dynamic regulation of trophic divergence are summarized, emphasizing common and contrasting hormonal and nitric oxide signaling strategies deployed in plant-pathogen interactions.

Programmed cell death (PCD) in multicellular organisms is a vital process in growth, development, and stress responses that contributes to the formation of tissues and organs. Although numerous studies have defined the molecular participants in apoptotic and PCD cascades, successful identification of early master regulators that target specific cells to live or die is limited. Using Zea mays somatic embryogenesis as a model system, we report that the expressions of two plant hemoglobin (Hb) genes (ZmHb1 and ZmHb2) regulate the cell survival/death decision that influences somatic embryogenesis through their cell-specific localization patterns. Suppression of either of the two ZmHbs is sufficient to induce PCD through a pathway initiated by elevated NO and Zn²⁺ levels and mediated by production of reactive oxygen species. The effect of the death program on the fate of the developing embryos is dependent on the localization patterns of the two ZmHbs. During somatic embryogenesis, ZmHb2 transcripts are restricted to a few cells anchoring the embryos to the subtending embryogenic tissue, whereas ZmHb1 transcripts extend to several embryonic domains. Suppression of ZmHb2 induces PCD in the anchoring cells, allowing the embryos to develop further, whereas suppression of ZmHb1 results in massive PCD, leading to abortion. We conclude that regulation of the expression of these ZmHbs has the capability to determine the developmental fate of the embryogenic tissue during somatic embryogenesis through their effect on PCD. This unique regulation might have implications for development and differentiation in other species.

Blackleg, caused by the fungal pathogen Leptosphaeria maculans, is one of the most economically important diseases of canola (Brassica napus, oilseed rape) worldwide. This study assessed incidence of blackleg, the avirulence allele, and mating type distributions of L. maculans isolates collected in commercial canola fields in Manitoba, Canada, from 2010 to 2015. A total of 956 L. maculans isolates were collected from 2010 to 2015 to determine the presence of 12 avirulence alleles using differential canola cultivars and/or PCR assays specific for each avirulence allele. AvrLm2, AvrLm4, AvrLm5, AvrLm6, AvrLm7, AvrLm11, and AvrLmS were detected at frequencies ranging from 97 to 33%, where the AvrLm1, AvrLm3, AvrLm9, AvrLepR1, and AvrLepR2 alleles were the least abundant. When the race structure was examined, a total of 170 races were identified among the 956 isolates, with three major races, AvrLm-2-4-5-6-7-11, AvrLm-2-4-5-6-7-11-S, and Avr-1-4-5-6-7-11-(S) accounting for 15, 10, and 6% of the total fungal population, respectively. The distribution of the mating type alleles (MAT1-1 and MAT1-2) indicated that sexual reproduction was not inhibited in any of the nine Manitoba regions in any of the years L. maculans isolates were collected.

Maintenance of a functional root is fundamental to plant survival in response to some abiotic stresses, such as water deficit. In this study, we found that overexpression of Arabidopsis class 1 phytoglobin (AtPgb1) alleviated the growth retardation of polyethylene glycol (PEG)-induced water stress by reducing programmed cell death (PCD) associated with protein folding in the endoplasmic reticulum (ER). This was in contrast to PEG-stressed roots down-regulating AtPgb1 that exhibited extensive PCD and reduced expression of several attenuators of ER stress, including BAX Inhibitor-1 (BI-1). The death program experienced by the suppression of AtPgb1 in stressed roots was mediated by reactive oxygen species (ROS) and ethylene. Suppression of ROS synthesis or ethylene perception reduced PCD and partially restored root growth. The PEG-induced cessation of root growth was preceded by structural changes in the root apical meristem (RAM), including the loss of cell and tissue specification, possibly as a result of alterations in PIN1- and PIN4-mediated auxin accumulation at the root pole. These events were attenuated by the overexpression of AtPgb1 and aggravated when AtPgb1 was suppressed. Specifically, suppression of AtPgb1 compromised the functionality of the WOX5-expressing quiescent cells (QCs), leading to the early and premature differentiation of the adjacent columella stem cells and to a rapid reduction in meristem size. The expression and localization of other root domain markers, such as SCARECROW (SCR), which demarks the endodermis and QCs, and WEREWOLF (WER), which specifies the lateral root cap, were also most affected in PEG-treated roots with suppressed AtPgb1. Collectively, the results demonstrate that AtPgb1 exercises a protective role in roots exposed to lethal levels of PEG, and suggest a novel function of this gene in ensuring meristem functionality through the retention of cell fate specification.

Genetic diversity is vital for the survival of any population. If humans were all the same, a single strain of a nasty flu virus, like COVID-19, could wipe us all out! In plants, genetic diversity plays a similar role. The variation in the type and number of resistance gene(s) between individuals can cause the difference between surviving a disease or not. Studies on genetic diversity will lead to the identification of novel disease-resistance genes. Canola (Brassica napus L.) is an economically and nutritionally important oilseed worldwide. Several serious diseases, including blackleg, clubroot, sclerotinia stem rot, and verticillium stripe, threaten canola production in Canada and worldwide. Traditional methods are not enough for effective control of these diseases. Therefore, the ideal approach is to optimize and utilize the resistance genes found in different B. napus cultivars. With the advent of next-generation sequencing and the development of genomics and molecular genetics techniques, it is now possible to rapidly identify and apply resistance genes. This paper reviews current information about disease-resistance genes identified in B. napus cultivars, mapping and cloning, their importance, role and function, and their association with plant disease resistance and application in resistance breeding. The feasibility of using current resistance sources in Canadian cultivars for developing new disease-resistant cultivars is also discussed. Sustainability of a farm and an agricultural system could be maintained by breeding for disease resistance, including the resistant varieties and incorporating other integrated pest management strategies along with it.

Proteins containing valine-glutamine (VQ) motifs play important roles in plant growth and development as well as in defense responses to both abiotic and biotic stresses. Blackleg disease, which is caused by Leptosphaeria maculans, is the most important disease in canola (Brassica napus) worldwide; however, the identification of Brassica napus VQs and their functions in response to blackleg disease have not yet been reported. In this study, we conducted a genome-wide identification and characterization of the VQ gene family in Brassica napus, including chromosome location, phylogenetic relations, gene structure, motif domain, synteny analysis, and cis-elements categorization of their promoter regions. To understand Brassica napus VQ gene function in response to blackleg disease, we overexpressed BnVQ7 (BnaA01g36880D, also known as the mitogen-activated protein kinase 4 substrate 1 [MKS1] gene) in a blackleg-susceptible canola variety, Westar. Overexpression of BnMKS1 in canola did not improve its resistance to blackleg disease at the seedling stage; however, transgenic canola plants overexpressing BnMKS1 displayed an enhanced resistance to L. maculans infection at the adult plant stage. Expression levels of downstream and defense marker genes in cotyledons increased significantly at the necrotrophic stage of L. maculans infection in the overexpression line of BnMKS1, suggesting that the salicylic acid- and jasmonic acid-mediated signaling pathways were both involved in the defense responses. Together, these results suggest that BnMKS1 might play an important role in defense against L. maculans.[ ] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .