@article{kim_van den broeck_karre_choi_christensen_wang_jo_cho_balint‐kurti_2021, title={Analysis of the transcriptomic, metabolomic, and gene regulatory responses to
            <i>Puccinia sorghi
            in maize}, volume={22}, ISSN={1464-6722 1364-3703}, url={http://dx.doi.org/10.1111/mpp.13040}, DOI={10.1111/mpp.13040}, abstractNote={Abstract Common rust, caused by Puccinia sorghi, is a widespread and destructive disease of maize. The Rp1‐D gene confers resistance to the P. sorghi IN2 isolate, mediating a hypersensitive cell death response (HR). To identify differentially expressed genes (DEGs) and metabolites associated with the compatible (susceptible) interaction and with Rp1‐D‐mediated resistance in maize, we performed transcriptomics and targeted metabolome analyses of P. sorghi IN2‐infected leaves from the near‐isogenic lines H95 and H95:Rp1‐D, which differed for the presence of Rp1‐D. We observed up‐regulation of genes involved in the defence response and secondary metabolism, including the phenylpropanoid, flavonoid, and terpenoid pathways. Metabolome analyses confirmed that intermediates from several transcriptionally up‐regulated pathways accumulated during the defence response. We identified a common response in H95:Rp1‐D and H95 with an additional H95:Rp1‐D‐specific resistance response observed at early time points at both transcriptional and metabolic levels. To better understand the mechanisms underlying Rp1‐D‐mediated resistance, we inferred gene regulatory networks occurring in response to P. sorghi infection. A number of transcription factors including WRKY53, BHLH124, NKD1, BZIP84, and MYB100 were identified as potentially important signalling hubs in the resistance‐specific response. Overall, this study provides a novel and multifaceted understanding of the maize susceptible and resistance‐specific responses to P. sorghi.}, number={4}, journal={Molecular Plant Pathology}, publisher={Wiley}, author={Kim, Saet‐Byul and Van den Broeck, Lisa and Karre, Shailesh and Choi, Hoseong and Christensen, Shawn A. and Wang, Guan‐Feng and Jo, Yeonhwa and Cho, Won Kyong and Balint‐Kurti, Peter}, year={2021}, month={Feb}, pages={465–479} }
 @article{karre_kim_kim_khangura_sermons_dilkes_johal_balint-kurti_2021, title={Maize Plants Chimeric for an Autoactive Resistance Gene Display a Cell-Autonomous Hypersensitive Response but Non–Cell Autonomous Defense Signaling}, volume={34}, ISSN={0894-0282 1943-7706}, url={http://dx.doi.org/10.1094/MPMI-04-20-0091-R}, DOI={10.1094/MPMI-04-20-0091-R}, abstractNote={The maize gene Rp1-D21 is a mutant form of the gene Rp1-D that confers resistance to common rust. Rp1-D21 triggers a spontaneous defense response that occurs in the absence of the pathogen and includes a programed cell death called the hypersensitive response (HR). Eleven plants heterozygous for Rp1-D21, in four different genetic backgrounds, were identified that had chimeric leaves with lesioned sectors showing HR abutting green non-lesioned sectors lacking HR. The Rp1-D21 sequence derived from each of the lesioned portions of leaves was unaltered from the expected sequence whereas the Rp1-D21 sequences from nine of the non-lesioned sectors displayed various mutations and we were unable to amplify Rp1-D21 from the other two non-lesioned sectors. In every case, the borders between the sectors were sharp with no transition zone, suggesting that HR and chlorosis associated with Rp1-D21 activity was cell-autonomous. Expression of defense response marker genes was assessed in the lesioned and non-lesioned sectors as well as in near-isogenic plants lacking and carrying Rp1-D21. Defense gene expression was somewhat elevated in non-lesioned sectors abutting sectors carrying Rp1-D21 compared to near-isogenic plants lacking Rp1-D21. This suggests that while the HR itself was cell autonomous, other aspects of the defense response initiated by Rp1-D21 were not.}, number={6}, journal={Molecular Plant-Microbe Interactions®}, publisher={Scientific Societies}, author={Karre, Shailesh and Kim, Saet-Byul and Kim, Bong-Suk and Khangura, Rajdeep S. and Sermons, Shannon M. and Dilkes, Brian and Johal, Guri and Balint-Kurti, Peter}, year={2021}, month={Jun}, pages={606–616} }
 @article{karre_kim_samira_balint‐kurti_2021, title={The maize ZmMIEL1 E3 ligase and ZmMYB83 transcription factor proteins interact and regulate the hypersensitive defence response}, volume={22}, ISSN={1464-6722 1364-3703}, url={http://dx.doi.org/10.1111/mpp.13057}, DOI={10.1111/mpp.13057}, abstractNote={Abstract The plant hypersensitive response (HR), a rapid cell death at the point of pathogenesis, is mediated by nucleotide‐binding site, leucine‐rich repeat (NLR) resistance proteins (R‐proteins) that recognize the presence of specific pathogen‐derived proteins. Rp1‐D21 is an autoactive maize NLR R‐protein that triggers HR spontaneously. We previously mapped loci associated with variation in the strength of HR induced by Rp1‐D21. Here we identify the E3 ligase ZmMIEL1 as the causal gene at a chromosome 10 modifier locus. Transient ZmMIEL1 expression in Nicotiana benthamiana reduced HR induced by Rp1‐D21, while suppression of ZmMIEL1 expression in maize carrying Rp1‐D21 increased HR. ZmMIEL1 also suppressed HR induced by another autoactive NLR, the Arabidopsis R‐protein RPM1D505V, in N. benthamiana. We demonstrated that ZmMIEL1 is a functional E3 ligase and that the effect of ZmMIEL1 was dependent on the proteasome but also that levels of Rp1‐D21 and RPM1D505V were not reduced when coexpressed with ZmMIEL1 in the N. benthamiana system. By comparison to a similar system in Arabidopsis, we identify ZmMYB83 as a potential target of ZmMIEL1. Suppression of ZmMYB83 expression in maize lines carrying Rp1‐D21 suppressed HR. Suppression of ZmMIEL1 expression caused an increase in ZmMYB83 transcript and protein levels in N. benthamiana and maize. Using coimmunoprecipitation and bimolecular fluorescence complementation assays, we demonstrated that ZmMIEL1 and ZmMYB83 physically interacted. Additionally, ZmMYB83 and ZmMIEL1 regulated the expression of a set of maize very long chain fatty acid (VLCFA) biosynthetic genes that may be involved in regulating HR.}, number={6}, journal={Molecular Plant Pathology}, publisher={Wiley}, author={Karre, Shailesh and Kim, Saet‐Byul and Samira, Rozalynne and Balint‐Kurti, Peter}, year={2021}, month={Apr}, pages={694–709} }
 @article{he_karre_johal_christensen_balint-kurti_2019, title={A maize polygalacturonase functions as a suppressor of programmed cell death in plants}, volume={19}, ISSN={1471-2229}, url={http://dx.doi.org/10.1186/s12870-019-1897-5}, DOI={10.1186/s12870-019-1897-5}, abstractNote={The hypersensitive defense response (HR) in plants is a fast, localized necrotic response around the point of pathogen ingress. HR is usually triggered by a pathogen recognition event mediated by a nucleotide-binding site, leucine-rich repeat (NLR) protein. The autoactive maize NLR gene Rp1-D21 confers a spontaneous HR response in the absence of pathogen recognition. Previous work identified a set of loci associated with variation in the strength of Rp1-D21-induced HR. A polygalacturonase gene homolog, here termed ZmPGH1, was identified as a possible causal gene at one of these loci on chromosome 7. Expression of ZmPGH1 inhibited the HR-inducing activity of both Rp1-D21 and that of another autoactive NLR, RPM1(D505V), in a Nicotiana benthamiana transient expression assay system. Overexpression of ZmPGH1 in a transposon insertion line of maize was associated with suppression of chemically-induced programmed cell death and with suppression of HR induced by Rp1-D21 in maize plants grown in the field. ZmPGH1 functions as a suppressor of programmed cell death induced by at least two autoactive NLR proteins and by two chemical inducers. These findings deepen our understanding of the control of the HR in plants.}, number={1}, journal={BMC Plant Biology}, publisher={Springer Science and Business Media LLC}, author={He, Yijian and Karre, Shailesh and Johal, Gurmukh S. and Christensen, Shawn A. and Balint-Kurti, Peter}, year={2019}, month={Jul} }
 @article{karre_kumar_yogendra_kage_kushalappa_charron_2019, title={HvWRKY23 regulates flavonoid glycoside and hydroxycinnamic acid amide biosynthetic genes in barley to combat Fusarium head blight}, volume={100}, ISSN={["1573-5028"]}, DOI={10.1007/s11103-019-00882-2}, abstractNote={Crop plant resistance against pathogens is governed by dynamic molecular and biochemical responses driven by complex transcriptional networks. However, the underlying mechanisms are largely unclear. Here we report an interesting role of HvWRKY23 transcription factor (TF) in modulating defense response against Fusarium head blight (FHB) in barley. The combined approach of gene silencing, metabolomics, real time expression analysis and ab initio bioinformatics tools led to the identification of the HvWRKY23 role in FHB resistance. The knock-down of HvWRKY23 gene in the FHB resistant barley genotype CI9831, followed by inoculation with Fusarium graminearum, led to the down regulation of key flavonoid and hydroxycinnamic acid amide biosynthetic genes resulting in reduced accumulation of resistant related (RR) secondary metabolites such as pelargonidin 3-rutinoside, peonidin 3-rhamnoside-5-glucoside, kaempferol 3-O-arabinoside and other flavonoid glycosides. Reduced abundances of RR metabolites in TF silenced plants were also associated with an increased proportion of spikelets diseased and amount of fungal biomass in spikelets, depicting the role of HvWRKY23 in disease resistance. The luciferase reporter assay demonstrated binding of HvWRKY23 protein to promoters of key flavonoid and hydroxycinnamic acid amides (HCAA) biosynthetic genes, such as HvPAL2, HvCHS1, HvHCT, HvLAC15 and HvUDPGT. The accumulation of high abundances of HCAAs and flavonoid glycosides reinforce cell walls to contain the pathogen to initial infection area. This gene in commercial cultivars can be edited, if non-functional, to enhance resistance against FHB.}, number={6}, journal={PLANT MOLECULAR BIOLOGY}, author={Karre, Shailesh and Kumar, Arun and Yogendra, Kalenahalli and Kage, Udaykumar and Kushalappa, Ajjamada and Charron, Jean-Benoit}, year={2019}, month={Aug}, pages={591–605} }