Potato NPH3/RPT2-like (NRL) member StNRL-9 interacts with Stphots and negatively regulates late blight resistance.

Blue light enhances the susceptibility of Nicotiana benthamiana to Phytophthora infestans, a causative agent of late blight disease. Investigating how blue light affects potato late blight resistance is an interesting aspect of exploring new ways to control late blight disease. Blue light photoreceptor phototropins (phot1, phot2) and their downstream interact protein StNRL1 have been shown to negatively regulate late blight resistance. In order to investigate whether other potato NPH3/RPT2-Like (NRL) family members are involved in regulating late blight resistance, this study focused on the potato NRL proteins containing RxSxS motif at the C-terminus. Another potato NRL protein StNRL-9, containing RxSxS motifs, was found to negatively regulate P. infestans resistance in potato and N. benthamiana. Overexpression of StNRL-9 in potato and N. benthamiana suppresses the accumulation of reactive oxygen species (ROS) and expression of the PTI marker genes NbWRKY7 and NbWRKY8. Similar to StNRL1, StNRL-9 interacts with the blue light receptors Stphot1 and Stphot2 on the cell membrane and could promote the degradation of a positive immune regulator StSWAP70. However StNRL-9 does not inhibit INF1-mediated cell death (ICD), which is different from the StNRL1 that inhibits ICD, indicating that both StNRL1 and StNRL-9 inhibit plant immunity in diverse ways. This study provides valuable information for further exploration of how plant phototropins and NRL family proteins regulate plant immunity.

Subfunctionalization of NRC3 altered the genetic structure of the Nicotiana NRC network.

Nucleotide-binding domain and leucine-rich repeat (NLR) proteins play crucial roles in immunity against pathogens in both animals and plants. In solanaceous plants, activation of several sensor NLRs triggers their helper NLRs, known as NLR-required for cell death (NRC), to form resistosome complexes to initiate immune responses. While the sensor NLRs and downstream NRC helpers display diverse genetic compatibility, molecular evolutionary events leading to the complex network architecture remained elusive. Here, we showed that solanaceous NRC3 variants underwent subfunctionalization after the divergence of Solanum and Nicotiana, altering the genetic architecture of the NRC network in Nicotiana. Natural solanaceous NRC3 variants form three allelic groups displaying distinct compatibilities with the sensor NLR Rpi-blb2. Ancestral sequence reconstruction and analyses of natural and chimeric variants identified six key amino acids involved in sensor-helper compatibility. These residues are positioned on multiple surfaces of the resting NRC3 homodimer, collectively contributing to their compatibility with Rpi-blb2. Upon activation, Rpi-blb2-compatible NRC3 variants form membrane-associated punctate and high molecular weight complexes, and confer resistance to the late blight pathogen Phytophthora infestans. Our findings revealed how mutations in NRC alleles lead to subfunctionalization, altering sensor-helper compatibility and contributing to the increased complexity of the NRC network.

SlLTPg1, a tomato lipid transfer protein, positively regulates in response to biotic stresses.

Late blight, caused by Phytophthora infestans (P. infestans), is among the most devastating diseases affecting tomato and other Solanaceae species. Lipid transfer proteins (LTPs) represent a class of small, basic proteins that play a crucial role in combating biotic stresses. Previous studies have shown that SlLTPg1 most strongly responds after P. infestans infestation among the LTPs family in tomato. However, the function of SlLTPg1 in disease resistance remains unclear. Here, we constructed transient overexpression and VIGS-silenced plants of SlLTPg1. Our results revealed that SlLTPg1 plays a regulatory role in enhancing tomato resistance against P. infestans. This enhancement was attributed to the upregulation of defense-related genes and reactive oxygen species (ROS) scavenging genes, as well as increased enzymatic antioxidant activities. Importantly, we found that the SlLTPg1 protein significantly inhibited the growth of Fusarium oxysporum (F. oxysporum) by observing the zone of inhibition. Interestingly, we found smaller lesion diameters and upregulated expression levels of PR genes in transient overexpression SlLTPg1 of tobacco. Therefore, we further constructed transgenic tobacco lines of SlLTPg1, presenting evidence that overexpression of SlLTPg1 could positively regulate the resistance of tobacco to F. oxysporum. These findings revealed the role of SlLTPg1 in tomato resistance to P. infestans and tobacco resistance to F. oxysporum. Moreover, we propose SlLTPg1 as a potential candidate gene for augmenting broad-spectrum plant resistance against pathogens.

Ribosomal S6 kinases 2 mediates potato resistance to late blight, through WRKY59 transcription factor.

Potato late blight is the most devastating pre- and post-harvest crop disease in the world, which is widespread and difficult to control, causing serious economic losses. Cultivating resistant varieties is a major way to prevent and control late blight in a green way. However, due to the rapid evolution of pathogens, the plant resistance is losing. Therefore, mining effective and durable genes involved in disease resistance is crucial for breeding resistant varieties against late blight. In this study, we took "potato-Phytophthora infestans" as the "host-pathogen" model system to discover the potential disease resistance-related genes and elucidate their molecular functional mechanism. Through yeast two-hybridization, bimolecular fluorescence complementation, Co-immunoprecipitation assays, and gene function validation etc., we found that ribosomal protein S6 kinase 2 (StS6K2) is a key resistant protein, which is interacted with StWRKY59 transcription factor. Overexpression of StS6K2 and StWRKY59 both enhanced the plants resistance to P. infestans, and promoted the host immune response, such as ROS burst and callose deposition. In OEStWRKY59 lines, DEGs involved in secondary metabolites synthesis, plant hormone signaling transduction and plant-pathogen interaction were significantly enriched. These findings provide novel genetic resources for the breeding of resistant varieties.

Evolution of Phytophthora infestans on its potato host since the Irish potato famine.

Phytophthora infestans is a major oomycete plant pathogen, responsible for potato late blight, which led to the Irish Potato Famine from 1845-1852. Since then, potatoes resistant to this disease have been bred and deployed worldwide. Their resistance (R) genes recognize pathogen effectors responsible for virulence and then induce a plant response stopping disease progression. However, most deployed R genes are quickly overcome by the pathogen. We use targeted sequencing of effector and R genes on herbarium specimens to examine the joint evolution in both P. infestans and potato from 1845-1954. Currently relevant effectors are historically present in P. infestans, but with alternative alleles compared to modern reference genomes. The historic FAM-1 lineage has the virulent Avr1 allele and the ability to break the R1 resistance gene before breeders deployed it in potato. The FAM-1 lineage is diploid, but later, triploid US-1 lineages appear. We show that pathogen virulence genes and host resistance genes have undergone significant changes since the Famine, from both natural and artificial selection.

Two structurally different oomycete lipophilic microbe-associated molecular patterns induce distinctive plant immune responses.

Plants recognize a variety of external signals and induce appropriate mechanisms to increase their tolerance to biotic and abiotic stresses. Precise recognition of attacking pathogens and induction of effective resistance mechanisms are critical functions for plant survival. Some molecular patterns unique to a certain group of microbes, microbe-associated molecular patterns (MAMPs), are sensed by plant cells as nonself molecules via pattern recognition receptors. While MAMPs of bacterial and fungal origin have been identified, reports on oomycete MAMPs are relatively limited. This study aimed to identify MAMPs from an oomycete pathogen Phytophthora infestans, the causal agent of potato late blight. Using reactive oxygen species (ROS) production and phytoalexin production in potato (Solanum tuberosum) as markers, two structurally different groups of elicitors, namely ceramides and diacylglycerols, were identified. P. infestans ceramides (Pi-Cer A, B, and D) induced ROS production, while diacylglycerol (Pi-DAG A and B), containing eicosapentaenoic acid (EPA) as a substructure, induced phytoalexins production in potato. The molecular patterns in Pi-Cers and Pi-DAGs essential for defense induction were identified as 9-methyl-4,8-sphingadienine (9Me-Spd) and 5,8,11,14-tetraene-type fatty acid (5,8,11,14-TEFA), respectively. These structures are not found in plants, but in oomycetes and fungi, indicating that they are microbe molecular patterns recognized by plants. When Arabidopsis (Arabidopsis thaliana) was treated with Pi-Cer D and EPA, partially overlapping but different sets of genes were induced. Furthermore, expression of some genes is upregulated only after the simultaneous treatment with Pi-Cer D and EPA, indicating that plants combine the signals from simultaneously recognized MAMPs to adapt their defense response to pathogens.

Alternative splicing of a potato disease resistance gene maintains homeostasis between growth and immunity.

Plants possess a robust and sophisticated innate immune system against pathogens and must balance growth with rapid pathogen detection and defense. The intracellular receptors with nucleotide-binding leucine-rich repeat (NLR) motifs recognize pathogen-derived effector proteins and thereby trigger the immune response. The expression of genes encoding NLR receptors is precisely controlled in multifaceted ways. The alternative splicing (AS) of introns in response to infection is recurrently observed but poorly understood. Here we report that the potato (Solanum tuberosum) NLR gene RB undergoes AS of its intron, resulting in 2 transcriptional isoforms, which coordinately regulate plant immunity and growth homeostasis. During normal growth, RB predominantly exists as an intron-retained isoform RB_IR, encoding a truncated protein containing only the N-terminus of the NLR. Upon late blight infection, the pathogen induces intron splicing of RB, increasing the abundance of RB_CDS, which encodes a full-length and active R protein. By deploying the RB splicing isoforms fused with a luciferase reporter system, we identified IPI-O1 (also known as Avrblb1), the RB cognate effector, as a facilitator of RB AS. IPI-O1 directly interacts with potato splicing factor StCWC15, resulting in altered localization of StCWC15 from the nucleoplasm to the nucleolus and nuclear speckles. Mutations in IPI-O1 that eliminate StCWC15 binding also disrupt StCWC15 re-localization and RB intron splicing. Thus, our study reveals that StCWC15 serves as a surveillance facilitator that senses the pathogen-secreted effector and regulates the trade-off between RB-mediated plant immunity and growth, expanding our understanding of molecular plant-microbe interactions.

Potato E3 ubiquitin ligase StRFP1 positively regulates late blight resistance by degrading sugar transporters StSWEET10c and StSWEET11.

Potato (Solanum tuberosum) is the fourth largest food crop in the world. Late blight, caused by oomycete Phytophthora infestans, is the most devastating disease threatening potato production. Previous research has shown that StRFP1, a potato Arabidopsis Tóxicos en Levadura (ATL) family protein, positively regulates late blight resistance via its E3 ligase activity. However, the underlying mechanism is unknown. Here, we reveal that StRFP1 is associated with the plasma membrane (PM) and undergoes constitutive endocytic trafficking. Its PM localization is essential for inhibiting P. infestans colonization. Through in vivo and in vitro assays, we investigated that StRFP1 interacts with two sugar transporters StSWEET10c and StSWEET11 at the PM. Overexpression (OE) of StSWEET10c or StSWEET11 enhances P. infestans colonization. Both StSWEET10c and StSWEET11 exhibit sucrose transport ability in yeast, and OE of StSWEET10c leads to an increased sucrose content in the apoplastic fluid of potato leaves. StRFP1 ubiquitinates StSWEET10c and StSWEET11 to promote their degradation. We illustrate a novel mechanism by which a potato ATL protein enhances disease resistance by degrading susceptibility (S) factors, such as Sugars Will Eventually be Exported Transporters (SWEETs). This offers a potential strategy for improving disease resistance by utilizing host positive immune regulators to neutralize S factors.

Lipid transfer protein StLTPa enhances potato disease resistance against different pathogens by binding and disturbing the integrity of pathogens plasma membrane.

Potato is the third most important food crop worldwide. Potato production suffers from severe diseases caused by multiple detrimental plant pathogens, and broad-spectrum disease resistance genes are rarely identified in potato. Here we identified the potato non-specific lipid transfer protein StLTPa, which enhances species none-specific disease resistance against various pathogens, such as the oomycete pathogen Phytophthora infestans, the fungal pathogens Botrytis cinerea and Verticillium dahliae, and the bacterial pathogens Pectobacterium carotovorum and Ralstonia solanacearum. The StLTPa overexpression potato lines do not show growth penalty. Furthermore, we provide evidence that StLTPa binds to lipids present in the plasma membrane (PM) of the hyphal cells of P. infestans, leading to an increased permeability of the PM. Adding of PI(3,5)P2 and PI(3)P could compete the binding of StLTPa to pathogen PM and reduce the inhibition effect of StLTPa. The lipid-binding activity of StLTPa is essential for its role in pathogen inhibition and promotion of potato disease resistance. We propose that StLTPa enhances potato broad-spectrum disease resistance by binding to, and thereby promoting the permeability of the PM of the cells of various pathogens. Overall, our discovery illustrates that increasing the expression of a single gene in potato enhances potato disease resistance against different pathogens without growth penalty.

The lncRNA20718-miR6022-RLPs module regulates tomato resistance to Phytophthora infestans.

KEY MESSAGE: Sl-lncRNA20718 acts as an eTM of Sl-miR6022 regulating its expression thereby affecting SlRLP6/10 expression. SlRLP6/10 regulate PRs expression, ROS accumulation, and JA/ET content thereby affecting tomato resistance to P. infestans. Tomato (Solanum lycopersicum) is an important horticultural and cash crop whose yield and quality can be severely affected by Phytophthora infestans (P. infestans). Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) are widely involved in plant defense responses against pathogens. The involvement of Sl-lncRNA20718 and Sl-miR6022 in tomato resistance to P. infestans as well as the targeting of Sl-miR6022 to receptor-like protein genes (RLPs) were predicted in our previous study. However, uncertainty exists regarding their potential interaction as well as the molecular processes regulating tomato resistance. Here, we found that Sl-lncRNA20718 and Sl-miR6022 are positive and negative regulators of tomato resistance to P. infestans by gain- and loss-of-function experiments, respectively. Overexpression of Sl-lncRNA20718 decreased the expression of Sl-miR6022, induced the expression of PRs, reduced the diameter of lesions (DOLs), thereby enhanced disease resistance. A six-point mutation in the binding region of Sl-lncRNA20718 to Sl-miR6022 disabled the interaction, indicating that Sl-lncRNA20718 acts as an endogenous target mimic (eTM) of Sl-miR6022. We demonstrated that Sl-miR6022 cleaves SlRLP6/10. Overexpression of Sl-miR6022 decreases the expression levels of SlRLP6/10, induces the accumulation of reactive oxygen species (ROS) and reduces the content of JA and ET, thus inhibiting tomato resistance to P. infestans. In conclusion, our study provides detailed information on the lncRNA20718-miR6022-RLPs module regulating tomato resistance to P. infestans by affecting the expression of disease resistance-related genes, the accumulation of ROS and the phytohormone levels, providing a new reference for tomato disease resistance breeding.

Recognition of pathogen-derived sphingolipids in Arabidopsis.

In plants, many invading microbial pathogens are recognized by cell-surface pattern recognition receptors, which induce defense responses. Here, we show that the ceramide Phytophthora infestans-ceramide D (Pi-Cer D) from the plant pathogenic oomycete P. infestans triggers defense responses in Arabidopsis. Pi-Cer D is cleaved by an Arabidopsis apoplastic ceramidase, NEUTRAL CERAMIDASE 2 (NCER2), and the resulting 9-methyl-branched sphingoid base is recognized by a plasma membrane lectin receptor-like kinase, RESISTANT TO DFPM-INHIBITION OF ABSCISIC ACID SIGNALING 2 (RDA2). 9-Methyl-branched sphingoid base is specific to microbes and induces plant immune responses by physically interacting with RDA2. Loss of RDA2 or NCER2 function compromised Arabidopsis resistance against an oomycete pathogen. Thus, we elucidated the recognition mechanisms of pathogen-derived lipid molecules in plants.

Genome-wide identification and characterization of the tomato F-box associated (FBA) protein family and expression analysis of their responsiveness to Phytophthora infestans.

Late blight caused by Phytophthora infestans brings huge economic losses to the production of tomato (Solanum lycopersicum) every year. F-box proteins participate in plants response to phytohormones and biotic stress, whereas as the largest subfamily of F-box superfamily, the detailed information about F-box associated (SlFBA) family in tomato has been rarely reported. In this study, a total of 46 tomato FBA genes were identified based on the latest genome annotation. Phylogenetic analysis revealed that the FBA proteins from tomato and 6 different plant species were clustered into 7 distinct clades. The SlFBA genes were unevenly distributed on 11 chromosomes of tomato, mainly concentrated in the regions with high gene density. Tandem duplications and purification selection contribute to the expansion and evolution of the SlFBA gene family. Transcriptome analysis revealed that the SlFBA genes were differentially expressed in different tissues with obvious tissue-specific expression patterns. There were 18 SlFBA genes differentially expressed in P. infestans-resistant and -susceptible tomato, among which, 3 SlFBA genes might play positive roles in tomato resistance to P. infestans. Taken together, this study systematically analyzed the SlFBA genes family for the first time and identified the candidate SlFBA genes that affect tomato resistance to P. infestans, which provided important genetic and breeding resources for improving tomato resistance to pathogens.

Heterologous overexpression of StERF3 triggers cell death in Nicotiana benthamiana.

Programmed cell death plays a crucial role in plant development and disease defense. Here, we report that the expression of StERF3, a potato EAR motif-containing transcription factor, promotes Phytophthora infestans colonization in Nicotiana benthamiana. Transient overexpression of StERF3 induces cell death in N. benthamiana leaves. The substitution of two key amino acids (14th and 19th) in its ERF domain (the DNA binding domain) dramatically altered its cell death-inducing ability. In addition, StERF3△EAR EAR motif-deletion or StERF3AAA mutation abolished the cell death-inducing ability. StERF3 interacted with the co-repressors Topless-related protein 1 (StTPL1) and Topless-related protein 3 (StTPL3) via the EAR motif. Moreover, cell death induced by StERF3 was facilitated by co-expression with StTPL1 or StTPL3. Virus-induced gene silencing (VIGS) of NbTPL1 and NbTPL3 in N. benthamiana compromised the cell death-inducing ability of StERF3. Furthermore, StERF3-induced cell death accompanied with ROS bursts and the upregulation of the respiratory burst oxidase homolog (Rboh) genes NbRbohA and NbRbohC. In addition, several cell death regulator genes, including NbCRTD, NbNCBP, and NbBCPL, and a hypersensitive cell death marker gene Hin1 were upregulated. StERF3 may positively regulate cell death through its EAR motif-mediated transcriptional repressor activity by inhibiting the expression of genes potentially coding the repressor of cell death (CD).

Overexpression of lncRNA08489 enhances tomato immunity against Phytophthora infestans by decoying miR482e-3p.

LncRNAs are widely involved in various biological processes of plants. Recent evidences indicated that lncRNAs could act as competing endogenous RNAs (ceRNAs) to adsorb complementary miRNAs in a type of target mimicry, thereby indirectly regulating the target genes of miRNAs. In this study, a lncRNA, lncRNA08489 was identified to be the ceRNA of miR482e-3p in tomato plants. The expression patterns of lncRNA08489 and miR482e-3p showed opposite trends after tomato plants infected with Phytophthora infestans. In tomato leaves overexpressing lncRNA08489 (OE08489), the expression level of miR482e-3p decreased and its target gene, NBS-LRR increased. After infection with P. infestans, the resistance of OE08489 plants was stronger than that of the wild type, and the reactive oxygen species (ROS) scavenging ability of OE08489 plants was significantly improved. Taken together, these results indicated that lncRNA08489 acted as a ceRNA to decoy miR482e-3p and regulate the expression of NBS-LRR to enhance tomato resistance through ROS-scavenging system.

NLR immune receptor RB is differentially targeted by two homologous but functionally distinct effector proteins.

Plant nucleotide-binding leucine-rich repeat (NLR) receptors mediate immune responses by directly or indirectly sensing pathogen-derived effectors. Despite significant advances in the understanding of NLR-mediated immunity, the mechanisms by which pathogens evolve to suppress NLR activation triggered by cognate effectors and gain virulence remain largely unknown. The agronomically important immune receptor RB recognizes the ubiquitous and highly conserved IPI-O RXLR family members (e.g., IPI-O1) from Phytophthora infestans, and this process is suppressed by the rarely present and homologous effector IPI-O4. Here, we report that self-association of RB via the coiled-coil (CC) domain is required for RB activation and is differentially affected by avirulence and virulence effectors. IPI-O1 moderately reduces the self-association of RB CC, potentially leading to changes in the conformation and equilibrium of RB, whereas IPI-O4 dramatically impairs CC self-association to prevent RB activation. We also found that IPI-O1 associates with itself, whereas IPI-O4 does not. Notably, IPI-O4 interacts with IPI-O1 and disrupts its self-association, therefore probably blocking its avirulence function. Furthermore, IPI-O4 enhances the interaction between RB CC and IPI-O1, possibly sequestering RB and IPI-O1 and subsequently blocking their interactions with signaling components. Taken together, these findings considerably extend our understanding of the underlying mechanisms by which emerging virulent pathogens suppress the NLR-mediated recognition of cognate effectors.

CRISPR/Cas9-Mediated SlMYBS2 Mutagenesis Reduces Tomato Resistance to Phytophthora infestans.

Phytophthora infestans (P. infestans) recently caused epidemics of tomato late blight. Our study aimed to identify the function of the SlMYBS2 gene in response to tomato late blight. To further investigate the function of SlMYBS2 in tomato resistance to P. infestans, we studied the effects of SlMYBS2 gene knock out. The SlMYBS2 gene was knocked out by CRISPR-Cas9, and the resulting plants (SlMYBS2 gene knockout, slmybs2-c) showed reduced resistance to P. infestans, accompanied by increases in the number of necrotic cells, lesion sizes, and disease index. Furthermore, after P. infestans infection, the expression levels of pathogenesis-related (PR) genes in slmybs2-c plants were significantly lower than those in wild-type (AC) plants, while the number of necrotic cells and the accumulation of reactive oxygen species (ROS) were higher than those in wild-type plants. Taken together, these results indicate that SlMYBS2 acts as a positive regulator of tomato resistance to P. infestans infection by regulating the ROS level and the expression level of PR genes.

Secreted pectin monooxygenases drive plant infection by pathogenic oomycetes.

The oomycete Phytophthora infestans is a damaging crop pathogen and a model organism to study plant-pathogen interactions. We report the discovery of a family of copper-dependent lytic polysaccharide monooxygenases (LPMOs) in plant pathogenic oomycetes and its role in plant infection by P. infestans We show that LPMO-encoding genes are up-regulated early during infection and that the secreted enzymes oxidatively cleave the backbone of pectin, a charged polysaccharide in the plant cell wall. The crystal structure of the most abundant of these LPMOs sheds light on its ability to recognize and degrade pectin, and silencing the encoding gene in P. infestans inhibits infection of potato, indicating a role in host penetration. The identification of LPMOs as virulence factors in pathogenic oomycetes opens up opportunities in crop protection and food security.

Visualising the ionome in resistant and susceptible plant-pathogen interactions.

At the morphological and anatomical levels, the ionome, or the elemental composition of an organism, is an understudied area of plant biology. In particular, the ionomic responses of plant-pathogen interactions are scarcely described, and there are no studies on immune reactions. In this study we explored two X-ray fluorescence (XRF)-based ionome visualisation methods (benchtop- and synchrotron-based micro-XRF [µXRF]), as well as the quantitative inductively coupled plasma optical emission spectroscopy (ICP-OES) method, to investigate the changes that occur in the ionome of compatible and incompatible plant-pathogen interactions. We utilised the agronomically important and comprehensively studied interaction between potato (Solanum tuberosum) and the late blight oomycete pathogen Phytophthora infestans as an example. We used one late blight-susceptible potato cultivar and two resistant transgenic plant lines (only differing from the susceptible cultivar in one or three resistance genes) both in control and P. infestans-inoculated conditions. In the lesions from the compatible interaction, we observed rearrangements of several elements, including a decrease of the mobile macronutrient potassium (K) and an increase in iron (Fe) and manganese (Mn), compared with the tissue outside the lesion. Interestingly, we observed distinctly different distribution patterns of accumulation at the site of inoculation in the resistant lines for calcium (Ca), magnesium (Mg), Mn and silicon (Si) compared to the susceptible cultivar. The results reveal different ionomes in diseased plants compared to resistant plants. Our results demonstrate a technical advance and pave the way for deeper studies of the plant-pathogen ionome in the future.

Chloroplasts alter their morphology and accumulate at the pathogen interface during infection by Phytophthora infestans.

Upon immune activation, chloroplasts switch off photosynthesis, produce antimicrobial compounds and associate with the nucleus through tubular extensions called stromules. Although it is well established that chloroplasts alter their position in response to light, little is known about the dynamics of chloroplast movement in response to pathogen attack. Here, we report that during infection with the Irish potato famine pathogen Phytophthora infestans, chloroplasts accumulate at the pathogen interface, associating with the specialized membrane that engulfs the pathogen haustorium. The chemical inhibition of actin polymerization reduces the accumulation of chloroplasts at pathogen haustoria, suggesting that this process is partially dependent on the actin cytoskeleton. However, chloroplast accumulation at haustoria does not necessarily rely on movement of the nucleus to this interface and is not affected by light conditions. Stromules are typically induced during infection, embracing haustoria and facilitating chloroplast interactions, to form dynamic organelle clusters. We found that infection-triggered stromule formation relies on BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1)-mediated surface immune signaling, whereas chloroplast repositioning towards haustoria does not. Consistent with the defense-related induction of stromules, effector-mediated suppression of BAK1-mediated immune signaling reduced stromule formation during infection. On the other hand, immune recognition of the same effector stimulated stromules, presumably via a different pathway. These findings implicate chloroplasts in a polarized response upon pathogen attack and point to more complex functions of these organelles in plant-pathogen interactions.

"Core" RxLR effectors in phytopathogenic oomycetes: A promising way to breeding for durable resistance in plants?

Phytopathogenic oomycetes are known to successfully infect their hosts due to their ability to secrete effector proteins. Of interest to many researchers are effectors with the N-terminal RxLR motif (Arginine-any amino acid-Leucine-Arginine). Owing to advances in genome sequencing, we can now comprehend the high level of diversity among oomycete effectors, and similarly, their conservation within and among species referred to here as "core" RxLR effectors (CREs). Currently, there is a considerable number of CREs that have been identified in oomycetes. Functional characterization of these CREs propose their virulence role with the potential of targeting central cellular processes that are conserved across diverse plant species. We reason that effectors that are highly conserved and recognized by the host, could be harnessed in engineering plants for durable as well as broad-spectrum resistance.