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1. ORA59 and EIN3 interaction couples jasmonate‐ethylene synergistic action to antagonistic salicylic acid regulation of PDF expression

   https://doi.org/10.1111/jipb.12524  

   He, Xiang ; Jiang, Jishan ; Wang, Chang‐Quan ; Dehesh, Katayoon ( April 2017 , Journal of Integrative Plant Biology)

   Hormonal crosstalk is central for tailoring plant responses to the nature of challenges encountered. The role of antagonism between the two major defense hormones, salicylic acid (SA) and jasmonic acid (JA), and modulation of this interplay by ethylene (ET) in favor of JA signaling pathway in plant stress responses is well recognized, but the underlying mechanism is not fully understood. Here, we show the opposing function of two transcription factors, ethylene insensitive3 (EIN3) and EIN3‐Like1 (EIL1), in SA‐mediated suppression and JA‐mediated activation ofPLANT DEFENSIN1.2(PDF1.2). This functional duality is mediated via their effect on protein, not transcript levels of thePDF1.2transcriptional activator octadecanoid‐responsiveArabidopsis59 (ORA59). Specifically, JA induces ORA59 protein levels independently of EIN3/EIL1, whereas SA reduces the protein levels dependently of EIN3/EIL1. Co‐infiltration assays revealed nuclear co‐localization of ORA59 and EIN3, and split‐luciferase together with yeast‐two‐hybrid assays established their physical interaction. The functional ramification of the physical interaction is EIN3‐dependent degradation of ORA59 by the 26S proteasome.

   These findings allude to SA‐responsive reduction of ORA59 levels mediated by EIN3 binding to and targeting of ORA59 for degradation, thus nominating ORA59 pool as a coordination node for the antagonistic function of ET/JA and SA.

    

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2. Maize resistance to insect herbivory is enhanced by silencing expression of genes for jasmonate‐isoleucine degradation using sugarcane mosaic virus

   https://doi.org/10.1002/pld3.407  

   Chung, Seung Ho ; Zhang, Shudi ; Song, Hojun ; Whitham, Steven A. ; Jander, Georg ( June 2022 , Plant Direct)

   Previously, sugarcane mosaic virus (SCMV) was developed as a vector for transient expression of heterologous genes inZea mays(maize). Here, we show that SCMV can also be applied for virus‐induced gene silencing (VIGS) of endogenous maize genes. Comparison of sense and antisense VIGS constructs targeting maizephytoene desaturase(PDS) showed that antisense constructs resulted in a greater reduction in gene expression. In a time course of gene expression after infection with VIGS constructs targetingPDS,lesion mimic 22(Les22), andIodent japonica 1(Ij1), efficient expression silencing was observed 2, 3, and 4 weeks after infection with SCMV. However, at Week 5, expression ofLes22andIj1was no longer significantly reduced compared with control plants. The defense signaling molecule jasmonate‐isoleucine (JA‐Ile) can be inactivated by 12C‐hydroxylation and hydrolysis, and knockout of these genes leads to herbivore resistance. JA‐Ile hydroxylases and hydrolases have been investigated in Arabidopsis, rice, andNicotiana attenuata. To determine whether the maize homologs of these genes function in plant defense, we silenced expression ofZmCYP94B1(predicted JA‐Ile hydroxylase) andZmJIH1(predicted JA‐Ile hydrolase) by VIGS with SCMV, which resulted in elevated expression of two defense‐related genes,Maize Proteinase Inhibitor(MPI) andRibosome Inactivating Protein 2(RIP2). AlthoughZmCYP94B1andZmJIH1gene expression silencing increased resistance toSpodoptera frugiperda(fall armyworm),Schistocerca americana(American birdwing grasshopper), andRhopalosiphum maidis(corn leaf aphid), there was no additive effect from silencing the expression of both genes. Further work will be required to determine the more precise functions of these enzymes in regulating maize defenses.

    

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3. A bacterial effector counteracts host autophagy by promoting degradation of an autophagy component

   https://doi.org/10.15252/embj.2021110352  

   Leong, Jia Xuan ; Raffeiner, Margot ; Spinti, Daniela ; Langin, Gautier ; Franz‐Wachtel, Mirita ; Guzman, Andrew R. ; Kim, Jung‐Gun ; Pandey, Pooja ; Minina, Alyona E. ; Macek, Boris ; et al ( May 2022 , The EMBO Journal)

   Beyond its role in cellular homeostasis, autophagy plays anti‐ and promicrobial roles in host–microbe interactions, both in animals and plants. One prominent role of antimicrobial autophagy is to degrade intracellular pathogens or microbial molecules, in a process termed xenophagy. Consequently, microbes evolved mechanisms to hijack or modulate autophagy to escape elimination. Although well‐described in animals, the extent to which xenophagy contributes to plant–bacteria interactions remains unknown. Here, we provide evidence thatXanthomonas campestrispv.vesicatoria (Xcv)suppresses host autophagy by utilizing type‐III effector XopL. XopL interacts with and degrades the autophagy component SH3P2 via its E3 ligase activity to promote infection. Intriguingly, XopL is targeted for degradation by defense‐related selective autophagy mediated by NBR1/Joka2, revealing a complex antagonistic interplay between XopL and the host autophagy machinery. Our results implicate plant antimicrobial autophagy in the depletion of a bacterial virulence factor and unravel an unprecedented pathogen strategy to counteract defense‐related autophagy in plant–bacteria interactions.

    

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4. On the initiation of jasmonate biosynthesis in wounded leaves

   https://doi.org/10.1093/plphys/kiac163  

   Kimberlin, Athen N. ; Holtsclaw, Rebekah E. ; Zhang, Tong ; Mulaudzi, Takalani ; Koo, Abraham J. ( April 2022 , Plant Physiology)

   The basal level of the plant defense hormone jasmonate (JA) in unstressed leaves is low, but wounding causes its near instantaneous increase. How JA biosynthesis is initiated is uncertain, but the lipolysis step that generates fatty acid precursors is generally considered to be the first step. Here, we used a series of physiological, pharmacological, genetic, and kinetic analyses of gene expression and hormone profiling to demonstrate that the early spiking of JA upon wounding does not depend on the expression of JA biosynthetic genes in Arabidopsis (Arabidopsis thaliana). Using a transgenic system, we showed how decoupling the responses to wounding and JA prevents the perpetual synthesis of JA in wounded leaves. We then used DEFECTIVE IN ANTHER DEHISCENCE1 (DAD1) as a model wound-responsive lipase to demonstrate that although its transient expression in leaves can elicit JA biosynthesis to a low level, an additional level of activation is triggered by wounding, which causes massive accumulation of JA. This wound-triggered boosting effect of DAD1-mediated JA synthesis can happen directly in damaged leaves or indirectly in undamaged remote leaves by the systemically transmitted wound signal. Finally, protein stability of DAD1 was influenced by wounding, α-linolenic acid, and mutation in its catalytic site. Together, the data support mechanisms that are independent of gene transcription and translation to initiate the rapid JA burst in wounded leaves and demonstrate how transient expression of the lipase can be used to reveal changes occurring at the level of activity and stability of the key lipolytic step.

    

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5. EXO70D isoforms mediate selective autophagic degradation of type-A ARR proteins to regulate cytokinin sensitivity

   https://doi.org/10.1073/pnas.2013161117  

   Acheampong, Atiako Kwame ; Shanks, Carly ; Cheng, Chia-Yi ; Schaller, G. Eric ; Dagdas, Yasin ; Kieber, Joseph J. ( October 2020 , Proceedings of the National Academy of Sciences)

   The phytohormone cytokinin influences many aspects of plant growth and development, several of which also involve the cellular process of autophagy, including leaf senescence, nutrient remobilization, and developmental transitions. TheArabidopsistype-A response regulators (type-A ARR) are negative regulators of cytokinin signaling that are transcriptionally induced in response to cytokinin. Here, we describe a mechanistic link between cytokinin signaling and autophagy, demonstrating that plants modulate cytokinin sensitivity through autophagic regulation of type-A ARR proteins. Type-A ARR proteins were degraded by autophagy in an AUTOPHAGY-RELATED (ATG)5-dependent manner, and this degradation is promoted by phosphorylation on a conserved aspartate in the receiver domain of the type-A ARRs. EXO70D family members interacted with type-A ARR proteins, likely in a phosphorylation-dependent manner, and recruited them to autophagosomes via interaction of the EXO70D AIM with the core autophagy protein, ATG8. Consistently, loss-of-functionexo70D1,2,3mutants exhibited compromised targeting of type-A ARRs to autophagic vesicles, have elevated levels of type-A ARR proteins, and are hyposensitive to cytokinin. Disruption of both type-AARRsandEXO70D1,2,3compromised survival in carbon-deficient conditions, suggesting interaction between autophagy and cytokinin responsiveness in response to stress. These results indicate that the EXO70D proteins act as selective autophagy receptors to target type-A ARR cargos for autophagic degradation, demonstrating modulation of cytokinin signaling by selective autophagy.

    

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