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Derepression of Ethylene-Stabilized Transcription Factors (EIN3/EIL1) Mediates Jasmonate and Ethylene Signaling Synergy in Arabidopsis

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Derepression of Ethylene-Stabilized Transcription Factors (EIN3/EIL1) Mediates Jasmonate and Ethylene Signaling Synergy in Arabidopsis Derepression of ethylene-stabilized transcription factors (EIN3/EIL1) mediates jasmonate and ethylene signaling synergy in Arabidopsis Ziqiang Zhua,1, Fengying Ana,1, Ying Fenga, Pengpeng Lia,2, Li Xueb,MuAa, Zhiqiang Jianga, Jong-Myong Kimc, Taiko Kim Toc, Wei Lib, Xinyan Zhanga, Qiang Yua, Zhi Donga, Wen-Qian Chena, Motoaki Sekic, Jian-Min Zhoub, and Hongwei Guoa,3 aState Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing 100871, China; bNational Institute of Biological Sciences, Beijing 102206, China; and cRIKEN Plant Science Center, Yokohama 2300045, Japan Edited by Mark Estelle, University of California at San Diego, La Jolla, CA, and approved June 9, 2011 (received for review March 11, 2011) Jasmonate (JA) and ethylene (ET) are two major plant hormones ETHYLENE INSENSITIVE 2 (EIN2), which is an essential that synergistically regulate plant development and tolerance to positive regulator in ET signaling (12). ETHYLENE IN- necrotrophic fungi. Both JA and ET induce the expression of SENSITIVE 3 (EIN3) and its closest homolog EIN3-LIKE 1 several pathogenesis-related genes, while blocking either signal- (EIL1) are two primary transcription factors downstream of ing pathway abolishes the induction of these genes by JA and ET EIN2 (6, 7, 13), which are necessary and sufficient for the in- – alone or in combination. However, the molecular basis of JA/ET duction of the vast majority of ethylene response genes (13 15). coaction and signaling interdependency is largely unknown. Here, In the absence of ET, EIN3/EIL1 are quickly degraded through we report that two Arabidopsis ET-stabilized transcription factors the action of two EIN3-binding F-box proteins 1 and 2 (EBF1 and EBF2), and ET enhances EIN3/EIL1 accumulation, prob- (EIN3 and EIL1) integrate ET and JA signaling in the regulation of – gene expression, root development, and necrotrophic pathogen ably through the repression of EBF1/2 (14, 16 18). JA is synthesized and conjugated with isoleucine to form the defense. Further studies reveal that JA enhances the transcrip- active hormone JA-Ile (19, 20), which is perceived by its receptor tional activity of EIN3/EIL1 by removal of JA-Zim domain (JAZ) CORONATINE INSENSITIVE 1 (COI1), an F-box protein PLANT BIOLOGY proteins, which physically interact with and repress EIN3/EIL1. In – fi (21 25). JASMONATE ZIM-DOMAIN (JAZ) proteins are addition, we nd that JAZ proteins recruit an RPD3-type histone transcriptional repressors, which interact with MYC2 transcrip- deacetylase (HDA6) as a corepressor that modulates histone acet- tion factor and repress its function (23, 26, 27). Recently, one ylation, represses EIN3/EIL1-dependent transcription, and inhibits possible mechanism underlying JAZ repression on MYC2 has JA signaling. Our studies identify EIN3/EIL1 as a key integration been demonstrated in that JAZ proteins associate with NOVEL node whose activation requires both JA and ET signaling, and INTERACTOR of JAZ (NINJA) to recruit TOPLESS as a co- illustrate transcriptional derepression as a common mechanism repressor to fulfill this function (28). The perception of JA-Ile to integrate diverse signaling pathways in the regulation of plant induces the interaction between COI1 and JAZs, which brings development and defense. JAZs for degradation and relieves their repression on MYC2 (23, 26). Two MYC2-like bHLH proteins (MYC3 and MYC4) root hair | Botrytis cinerea were also able to interact with JAZs and act addictively with MYC2 in mediating a subset of JA-regulated responses, including lants are sessile organisms and face different environmental inhibition of root elongation, wound response, and metabolism Pchanges during their lifespan. To survive various abiotic and (29–31). Besides MYC2/MYC3/MYC4, two MYB transcription biotic stresses, plants synthesize a number of small molecules factors (MYB21 and MYB24) were recently identified as JAZ functioning as phytohormones to elaborately regulate their growth, targets in regulating plant stamen development (32). development, and defense. Two types of phytohormones— Histone deacetylation, which is catalyzed by histone deacety- ethylene (ET) and jasmonate (JA)—are crucial for plant de- lases (HDAs), is a type of chromatin modification commonly velopment and defense against necrotrophic fungi infections (1– associated with transcriptional repression (33). It has been 3). Complicated modes of interaction between ET and JA have reported that histone deacetylation affects many growth and been documented in different processes. For example, ET developmental events in plants, such as flowering time, cold strongly suppresses JA-induced wounding-responsive gene ex- tolerance, embryogenesis, root hair development, abscisic acid, pression, but JA suppresses ET-induced apical hook formation and salt responses (34–38). A molecular link between this epi- (4, 5), indicative of their antagonisms. Upon necrotrophic fungi genetic control and JA signaling has been implied, as an RPD3- infections, plants can quickly produce ET and JA and induce the type histone deacetylase 6 (HDA6) was reported to associate expression of downstream defense genes (like ERF1, ORA59, with COI1 in a coimmunoprecipitation (co-IP) assay (39). It was and PDF1.2) that help plants tolerate or fight against the fungal also found that the transcript levels of some JA-responsive genes pathogens (1). Plants treated with exogenous JA or ET express are altered in HDA6 or HDA19 loss-of-function mutants and high levels of defense genes (6, 7), and simultaneous treatment with JA and ET results in the highest expression (8). Neverthe- less, in the ET or JA insensitive mutant (ein2 or coi1, re- Author contributions: Z.Z. and H.G. designed research; Z.Z., F.A., Y.F., P.L., L.X., M.A., W.L., spectively), JA and ET alone or in combination fail to induce the X.Z., Q.Y., and Z.D. performed research; J.-M.K., T.K.T., W.-Q.C., and M.S. contributed new expression of those defense genes (8, 9), indicating that the two reagents/analytic tools; Z.Z., Z.J., J.-M.Z., and H.G. analyzed data; and Z.Z. and H.G. wrote hormone-signaling pathways are required concomitantly for the the paper. activation of plant-defense response. These results suggest that The authors declare no conflict of interest. JA and ET act synergistically and mutually dependently in reg- This article is a PNAS Direct Submission. ulating necrotrophic pathogen responses. However, the molec- 1 ular details underlying such hormone synergy and signaling Z.Z. and F.A. contributed equally to this work. interdependency are currently unknown. 2Present address: Department of Biology, Stanford University, Stanford, CA 94305. ET is a gaseous hormone, which is perceived by its receptors 3To whom correspondence should be addressed. E-mail: [email protected]. and represses a Raf-like kinase CONSTITUTIVE ETHYL- This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10. ENE RESPONSE 1 (CTR1) (10, 11). Downstream of CTR1 is 1073/pnas.1103959108/-/DCSupplemental. www.pnas.org/cgi/doi/10.1073/pnas.1103959108 PNAS Early Edition | 1of6 Downloaded by guest on September 30, 2021 transgenic overexpression plants (40, 41). However, the action of induce root hair development (43). However, such induction in these HDAs in JA signaling is not clear. ein3 eil1 was largely abolished (Fig. 1 C and D). We also found Here, we report that EIN3 and EIL1 integrate ET and JA that ein3 eil1 was partially insensitive in JA-induced inhibition of signaling in plant development and defense against necrotrophic root elongation (Fig. 1E). Conversely, transgenic plants over- pathogens. JAZ proteins directly interact with EIN3/EIL1 and expressing EIN3 or EIL1 (EIN3ox or EIL1ox) (6) were hyper- recruit HDA6 as a corepressor to repress the transcriptional ac- sensitive to JA in root-growth inhibition (Fig. 1F). On the other tivity of EIN3/EIL1. Our work defines EIN3/EIL1 as a previously hand, ein3 eil1 was indistinguishable from WT in terms of fertility unexplored class of JAZ-associated transcription factors that are and JA-induced anthocyanin biosynthesis (Fig. S2). Collectively, subject to JAZ repression via the action of histone deacetylation, we conclude that EIN3 and EIL1 are positive regulators of and provides unique insights into how plant hormones co- a subset of JA responses, including pathogenesis-related gene ordinately regulate plant development and defense response. expression, plant resistance to necrotrophic fungi, and root de- velopment, but not fertility and pigment metabolism. Results EIN3/EIL1 Are Positive Regulators Mediating a Subset of JA Responses. JAZ Proteins Interact with EIN3/EIL1. To understand how EIN3/ Previous studies have revealed that JA alone or in combination EIL1 mediate JA signaling, we speculated that EIN3 and EIL1 with ET fails to induce pathogenesis-related genes (such as might be targeted by JAZ proteins, and thus tested the in- ERF1, ORA59, PDF1.2)inein2 background (8, 9). Because ein3 teraction between JAZ proteins and EIN3/EIL1. We found that eil1 is phenotypically similar to ein2 and one of ET/JA-regulated JAZ1 interacted with EIN3 in yeast cells, and an EIN3 fragment genes (ERF1) is a direct target of EIN3 (7, 13), we hypothesized containing amino acid residues 200 to 500 was sufficient for that EIN3 and EIL1 may function as key transcriptional regu- JAZ1 binding (Fig. 2A). The interaction between JAZ1 and an lators of JA/ET-induced gene expression. We first examined the EIL1 fragment (amino acids 201–501) was also observed (Fig. induction of JA-responsive genes in ein3 eil1 upon JA treatment. S3A). To test if EIN3/EIL1 interacts with other JAZ proteins, we The JA induction of pathogenesis-related genes (ERF1, ORA59, chose JAZ3 and JAZ9 and found that both JAZ3 and JAZ9 and PDF1.2) was abolished in ein3 eil1, but the expression of were able to interact with EIN3 (amino acids 200–500) and EIL1 wound-response genes (e.g., VSP2) that are regulated by MYC2 (amino acids 201–501) in yeast cells (Fig.
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