Plants are sessile and have to cope with environmentally induced damage through modification of growth and defense pathways. It is an open question how tissue regeneration is triggered in such responses and whether this involves stem cell activation. The stress hormone jasmonate (JA) plays well-established roles in wounding and defense responses. JA also affects growth which is hitherto interpreted as trade-off between growth and defense. Here, we describe a molecular network triggered by wound-induced JA that promotes stem cell activation and regeneration. JA regulates organizer cell activity in the root stem cell niche through the RBR-SCR network and stress response protein ERF115. Moreover, JA-induced ERF109 transcription stimulates CYCD6;1 expression, functions upstream of ERF115 and promotes regeneration. Soil penetration and response to nematode herbivory induce and require this JA mediated regeneration response. Therefore, the JA tissue damage response pathway induces stem cell activation and regeneration, and activates growth after environmental stress. Results JA acts through RBR-SCR to regulate quiescenceWe confirmed that JA promotes division of QC cells (Chen et al., 2011) ( Figures 1A and 1B, S1B and S1C), and that extra QC divisions occur in plants with altered SCR-RBR network:pWOX5::amiGORBR, which specifically downregulates RBR in the QC, and pSCR::SCRaca-YFP, which specifically disrupts RBR-SCR protein interaction (Cruz-Ramirez et al., 2013) ( Figures 1D and 1G). We observed QC divisions in wild type Col-0 after 50 µM or 100 µM MeJA (methyl ester of JA) treatment for 48 hours ( Figures 1A-1C and 1J), respectively. Conversely, no extra QC divisions were detected in pWOX5::amiGORBR and pSCR::SCRaca-YFP lines treated with 50 µM or 100 µM MeJA for the same period (Figures 1D-1I and 1K-1L), suggesting that JA may function through the SCR-RBR network in regulating quiescence of QC. To further confirm this, we introgressed the JA receptor loss of function mutant allele coi1-2 (Xu et al., 2002) into pWOX5::amiGORBR and pSCR::SCRaca-YFP lines. The QC division phenotypes and QC cell numbers of these introgression lines revealed no differences to pSCR::SCRaca-YFP and pWOX5::amiGORBR lines, both with and without MeJA treatment, respectively ( Figures S1D-S1M). These findings position SCR and RBR downstream of COI1 to control quiescence of QC. After MeJA treatment, QC cell numbers of scr-3 and shr-2 mutants did not increase significantly compared to controls ( Figures S1N-S1T), confirming that JA induces QC division through the SCR/SHR pathway. SCR and RBR expression levels were not altered significantly after MeJA treatment, judged by marker expression and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays (Figures S1U-S1AA).These data indicate that JA does not regulate SCR and RBR at the gene expression level. JA directly induces ERF115 transcriptionThe AP2/ERF family transcription factor ERF115 was reported to control root QC cell division (Heyman et al., 2013). When 35S::ERF11...
Plants lack the seemingly unlimited receptor diversity of a somatic adaptive immune system as found in vertebrates and rely on only a relatively small set of innate immune receptors to resist a myriad of pathogens. Here, we show that disease-resistant tomato plants use an efficient mechanism to leverage the limited nonself recognition capacity of their innate immune system. We found that the extracellular plant immune receptor protein Cf-2 of the red currant tomato (Solanum pimpinellifolium) has acquired dual resistance specificity by sensing perturbations in a common virulence target of two independently evolved effectors of a fungus and a nematode. The Cf-2 protein, originally identified as a monospecific immune receptor for the leaf mold fungus Cladosporium fulvum, also mediates disease resistance to the root parasitic nematode Globodera rostochiensis pathotype Ro1-Mierenbos. The Cf-2-mediated dual resistance is triggered by effector-induced perturbations of the apoplastic Rcr3 pim protein of S. pimpinellifolium. Binding of the venom allergen-like effector protein Gr-VAP1 of G. rostochiensis to Rcr3 pim perturbs the active site of this papain-like cysteine protease. In the absence of the Cf-2 receptor, Rcr3 pim increases the susceptibility of tomato plants to G. rostochiensis, thus showing its role as a virulence target of these nematodes. Furthermore, both nematode infection and transient expression of Gr-VAP1 in tomato plants harboring Cf-2 and Rcr3 pim trigger a defense-related programmed cell death in plant cells. Our data demonstrate that monitoring host proteins targeted by multiple pathogens broadens the spectrum of disease resistances mediated by single plant immune receptors.parasitism | secretions | SCP/TAPS proteins | hypersensitive response
The potato cyst nematode Globodera rostochiensis invades roots of host plants where it transforms cells near the vascular cylinder into a permanent feeding site. The host cell modifications are most likely induced by a complex mixture of proteins in the stylet secretions of the nematodes. Resistance to nematodes conferred by nucleotide-binding-leucine-rich repeat (NB-LRR) proteins usually results in a programmed cell death in and around the feeding site, and is most likely triggered by the recognition of effectors in stylet secretions. However, the actual role of these secretions in the activation and suppression of effector-triggered immunity is largely unknown. Here we demonstrate that the effector SPRYSEC-19 of G. rostochiensis physically associates in planta with the LRR domain of a member of the SW5 resistance gene cluster in tomato (Lycopersicon esculentum).
Despite causing considerable damage to host tissue during the onset of parasitism, nematodes establish remarkably persistent infections in both animals and plants. It is thought that an elaborate repertoire of effector proteins in nematode secretions suppresses damage-triggered immune responses of the host. However, the nature and mode of action of most immunomodulatory compounds in nematode secretions are not well understood. Here, we show that venom allergen-like proteins of plant-parasitic nematodes selectively suppress host immunity mediated by surface-localized immune receptors. Venom allergen-like proteins are uniquely conserved in secretions of all animal- and plant-parasitic nematodes studied to date, but their role during the onset of parasitism has thus far remained elusive. Knocking-down the expression of the venom allergen-like protein Gr-VAP1 severely hampered the infectivity of the potato cyst nematode Globodera rostochiensis. By contrast, heterologous expression of Gr-VAP1 and two other venom allergen-like proteins from the beet cyst nematode Heterodera schachtii in plants resulted in the loss of basal immunity to multiple unrelated pathogens. The modulation of basal immunity by ectopic venom allergen-like proteins in Arabidopsis thaliana involved extracellular protease-based host defenses and non-photochemical quenching in chloroplasts. Non-photochemical quenching regulates the initiation of the defense-related programmed cell death, the onset of which was commonly suppressed by venom allergen-like proteins from G. rostochiensis, H. schachtii, and the root-knot nematode Meloidogyne incognita. Surprisingly, these venom allergen-like proteins only affected the programmed cell death mediated by surface-localized immune receptors. Furthermore, the delivery of venom allergen-like proteins into host tissue coincides with the enzymatic breakdown of plant cell walls by migratory nematodes. We, therefore, conclude that parasitic nematodes most likely utilize venom allergen-like proteins to suppress the activation of defenses by immunogenic breakdown products in damaged host tissue.
Expression of polygalacturonase-inhibiting protein (PGIP) genes and production of oligogalacturonides (OGs) form an important component of plant basal resistance against cyst nematodes, but not root-knot nematodes.
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