scholarly journals The Barley HvWRKY6 Transcription Factor Is Required for Resistance Against Pyrenophora teres f. teres

2021 ◽  
Vol 11 ◽  
Author(s):  
Prabin Tamang ◽  
Jonathan K. Richards ◽  
Shyam Solanki ◽  
Gazala Ameen ◽  
Roshan Sharma Poudel ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Defense Mechanisms ◽  
Fungal Pathogens ◽  
Global Climate ◽  
Effective Resistance ◽  
Exome Capture ◽  
Transcriptional Gene Silencing ◽  
Pyrenophora Teres ◽  
Necrotrophic Pathogen ◽  
Barley Line

Barley is an important cereal crop worldwide because of its use in the brewing and distilling industry. However, adequate supplies of quality malting barley are threatened by global climate change due to drought in some regions and excess precipitation in others, which facilitates epidemics caused by fungal pathogens. The disease net form net blotch caused by the necrotrophic fungal pathogen Pyrenophora teres f. teres (Ptt) has emerged as a global threat to barley production and diverse populations of Ptt have shown a capacity to overcome deployed genetic resistances. The barley line CI5791 exhibits remarkably effective resistance to diverse Ptt isolates from around the world that maps to two major QTL on chromosomes 3H and 6H. To identify genes involved in this effective resistance, CI5791 seed were γ-irradiated and two mutants, designated CI5791-γ3 and CI5791-γ8, with compromised Ptt resistance were identified from an M2 population. Phenotyping of CI5791-γ3 and -γ8 × Heartland F2 populations showed three resistant to one susceptible segregation ratios and CI5791-γ3 × -γ8 F1 individuals were susceptible, thus these independent mutants are in a single allelic gene. Thirty-four homozygous mutant (susceptible) CI5791-γ3 × Heartland F2 individuals, representing 68 recombinant gametes, were genotyped via PCR genotype by sequencing. The data were used for single marker regression mapping placing the mutation on chromosome 3H within an approximate 75 cM interval encompassing the 3H CI5791 resistance QTL. Sequencing of the mutants and wild-type (WT) CI5791 genomic DNA following exome capture identified independent mutations of the HvWRKY6 transcription factor located on chromosome 3H at ∼50.7 cM, within the genetically delimited region. Post transcriptional gene silencing of HvWRKY6 in barley line CI5791 resulted in Ptt susceptibility, confirming that it functions in NFNB resistance, validating it as the gene underlying the mutant phenotypes. Allele analysis and transcript regulation of HvWRKY6 from resistant and susceptible lines revealed sequence identity and upregulation upon pathogen challenge in all genotypes analyzed, suggesting a conserved transcription factor is involved in the defense against the necrotrophic pathogen. We hypothesize that HvWRKY6 functions as a conserved signaling component of defense mechanisms that restricts Ptt growth in barley.

scholarly journals A combinatorial action of GmMYB176 and GmbZIP5 controls isoflavonoid biosynthesis in soybean (Glycine max)

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Arun Kumaran Anguraj Vadivel ◽  
Tim McDowell ◽  
Justin B. Renaud ◽  
Sangeeta Dhaubhadel
Keyword(s):  
Transcription Factor ◽  
Hairy Roots ◽  
Defense Mechanisms ◽  
Biosynthetic Pathway ◽  
Bzip Transcription Factor ◽  
Myb Transcription Factor ◽  
In Planta ◽  
Rnai Silencing ◽  
Protein Protein Interaction ◽  
Soybean Roots

AbstractGmMYB176 is an R1 MYB transcription factor that regulates multiple genes in the isoflavonoid biosynthetic pathway, thereby affecting their levels in soybean roots. While GmMYB176 is important for isoflavonoid synthesis, it is not sufficient for the function and requires additional cofactor(s). The aim of this study was to identify the GmMYB176 interactome for the regulation of isoflavonoid biosynthesis in soybean. Here, we demonstrate that a bZIP transcription factor GmbZIP5 co-immunoprecipitates with GmMYB176 and shows protein–protein interaction in planta. RNAi silencing of GmbZIP5 reduced the isoflavonoid level in soybean hairy roots. Furthermore, co-overexpression of GmMYB176 and GmbZIP5 enhanced the level of multiple isoflavonoid phytoallexins including glyceollin, isowighteone and a unique O-methylhydroxy isoflavone in soybean hairy roots. These findings could be utilized to develop biotechnological strategies to manipulate the metabolite levels either to enhance plant defense mechanisms or for human health benefits in soybean or other economically important crops.

scholarly journals Investigation of Antifungal Mechanisms of Thymol in the Human Fungal Pathogen, Cryptococcus neoformans

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3476
Author(s):  
Kwang-Woo Jung ◽  
Moon-Soo Chung ◽  
Hyoung-Woo Bai ◽  
Byung Yeoup Chung ◽  
Sungbeom Lee
Keyword(s):  
Cryptococcus Neoformans ◽  
Fungal Pathogens ◽  
Reverse Genetics ◽  
Mapk Pathway ◽  
Global Climate ◽  
Mitogen Activated Protein Kinase ◽  
Ergosterol Biosynthesis ◽  
Thymus Vulgaris ◽  
Dependent Manner ◽  
Expression Levels

Due to lifespan extension and changes in global climate, the increase in mycoses caused by primary and opportunistic fungal pathogens is now a global concern. Despite increasing attention, limited options are available for the treatment of systematic and invasive mycoses, owing to the evolutionary similarity between humans and fungi. Although plants produce a diversity of chemicals to protect themselves from pathogens, the molecular targets and modes of action of these plant-derived chemicals have not been well characterized. Using a reverse genetics approach, the present study revealed that thymol, a monoterpene alcohol from Thymus vulgaris L., (Lamiaceae), exhibits antifungal activity against Cryptococcus neoformans by regulating multiple signaling pathways including calcineurin, unfolded protein response, and HOG (high-osmolarity glycerol) MAPK (mitogen-activated protein kinase) pathways. Thymol treatment reduced the intracellular concentration of Ca2+ by controlling the expression levels of calcium transporter genes in a calcineurin-dependent manner. We demonstrated that thymol decreased N-glycosylation by regulating the expression levels of genes involved in glycan-mediated post-translational modifications. Furthermore, thymol treatment reduced endogenous ergosterol content by decreasing the expression of ergosterol biosynthesis genes in a HOG MAPK pathway-dependent manner. Collectively, this study sheds light on the antifungal mechanisms of thymol against C. neoformans.

scholarly journals Disruption of barley immunity to powdery mildew by an in-frame Lys-Leu deletion in the essential protein SGT1

Genetics ◽  
2020 ◽  
Vol 217 (2) ◽  
Author(s):  
Antony V E Chapman ◽  
Matthew Hunt ◽  
Priyanka Surana ◽  
Valeria Velásquez-Zapata ◽  
Weihui Xu ◽  
...  
Keyword(s):  
Powdery Mildew ◽  
Fungal Pathogens ◽  
Novel Mutation ◽  
Exome Capture ◽  
Resistance Locus ◽  
Hordeum Vulgare L ◽  
Powdery Mildew Fungus ◽  
Pathogen Effectors ◽  
Cell Processes ◽  
Disease Resistances

Abstract Barley (Hordeum vulgare L.) Mla (Mildew resistance locus a) and its nucleotide-binding, leucine-rich-repeat receptor (NLR) orthologs protect many cereal crops from diseases caused by fungal pathogens. However, large segments of the Mla pathway and its mechanisms remain unknown. To further characterize the molecular interactions required for NLR-based immunity, we used fast-neutron mutagenesis to screen for plants compromised in MLA-mediated response to the powdery mildew fungus, Blumeria graminis f. sp. hordei. One variant, m11526, contained a novel mutation, designated rar3 (required for Mla6 resistance3), that abolishes race-specific resistance conditioned by the Mla6, Mla7, and Mla12 alleles, but does not compromise immunity mediated by Mla1, Mla9, Mla10, and Mla13. This is analogous to, but unique from, the differential requirement of Mla alleles for the co-chaperone Rar1 (required for Mla12 resistance1). We used bulked-segregant-exome capture and fine mapping to delineate the causal mutation to an in-frame Lys-Leu deletion within the SGS domain of SGT1 (Suppressor of G-two allele of Skp1, Sgt1ΔKL308–309), the structural region that interacts with MLA proteins. In nature, mutations to Sgt1 usually cause lethal phenotypes, but here we pinpoint a unique modification that delineates its requirement for some disease resistances, while unaffecting others as well as normal cell processes. Moreover, the data indicate that the requirement of SGT1 for resistance signaling by NLRs can be delimited to single sites on the protein. Further study could distinguish the regions by which pathogen effectors and host proteins interact with SGT1, facilitating precise editing of effector incompatible variants.

scholarly journals The Effect of Transcription Factor MYB14 on Defense Mechanisms in Vitis quinquangularis-Pingyi

2020 ◽  
Vol 21 (3) ◽  
pp. 706 ◽  
Author(s):  
Yangyang Luo ◽  
Qingyang Wang ◽  
Ru Bai ◽  
Ruixiang Li ◽  
Lu Chen ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Nicotiana Benthamiana ◽  
Defense Mechanisms ◽  
Qualitative Difference ◽  
Defense Responses ◽  
Molecular Pattern ◽  
Effector Triggered Immunity ◽  
Pathogen Associated Molecular Pattern ◽  
Basal Immunity ◽  
Stilbene Biosynthesis

In the current study, we identified a transcription factor, MYB14, from Chinese wild grape, Vitis quinquangularis-Pingyi (V. quinquangularis-PY), which could enhance the main stilbene contents and expression of stilbene biosynthesis genes (StSy/RS) by overexpression of VqMYB14. The promoter of VqMYB14 (pVqMYB14) was shown to be induced as part of both basal immunity (also called pathogen-associated molecular pattern (PAMP)-triggered immunity, PTI) and effector-triggered immunity (ETI), triggered by the elicitors flg22 and harpin, respectively. This was demonstrated by expression of pVqMYB14 in Nicotiana benthamiana and Vitis. We identified sequence differences, notably an 11 bp segment in pVqMYB14 that is important for the PTI/ETI, and particularly for the harpin-induced ETI response. In addition, we showed that activation of the MYB14 promoter correlates with differences in the expression of MYB14 and stilbene pattern induced by flg22 and harpin. An experimental model of upstream signaling in V. quinquangularis-PY is presented, where early defense responses triggered by flg22 and harpin partially overlap, but where the timing and levels differ. This translates into a qualitative difference with respect to patterns of stilbene accumulation.

scholarly journals Ethylene-Responsive AP2/ERF Transcription Factor MACD1 Participates in Phytotoxin-Triggered Programmed Cell Death

2013 ◽  
Vol 26 (8) ◽  
pp. 868-879 ◽  
Author(s):  
Keisuke Mase ◽  
Nobuaki Ishihama ◽  
Hitoshi Mori ◽  
Hideki Takahashi ◽  
Hironori Kaminaka ◽  
...  
Keyword(s):  
Cell Death ◽  
Transcription Factor ◽  
Programmed Cell Death ◽  
Fumonisin B1 ◽  
Structural Analog ◽  
Necrotrophic Pathogen ◽  
Factors Affecting ◽  
Downstream Signaling ◽  
Upregulated Genes ◽  
Erf Transcription Factor

To investigate plant programmed cell death (PCD), we developed the model system using phytotoxin AAL, which is produced by necrotrophic pathogen Alternaria alternata f. sp. lycopersici, and AAL-sensitive Nicotiana umbratica. We previously reported that ethylene (ET) signaling plays a pivotal role in AAL-triggered cell death (ACD). However, downstream signaling of ET to ACD remains unclear. Here, we show that the modulator of AAL cell death 1 (MACD1), which is an APETALA2/ET response factor (ERF) transcription factor, participates in ACD and acts downstream of ET signaling during ACD. MACD1 is a transcriptional activator and MACD1 overexpression plants showed earlier ACD induction than control plants, suggesting that MACD1 positively regulates factors affecting cell death. To investigate the role of MACD1 in PCD, we used Arabidopsis thaliana and a structural analog of AAL, fumonisin B1 (FB1). FB1-triggered cell death was compromised in ET signaling and erf102 mutants. The loh2 mutants showed sensitivity to AAL, and the loh2-1/erf102 double mutant compromised ACD, indicating that ERF102 also participates in ACD. To investigate the PCD-associated genes regulated by ERF102, we compared our microarray data using ERF102 overexpression plants with the database of upregulated genes by AAL treatment in loh2 mutants, and found genes under the control of ERF102 in ACD.

scholarly journals GATA Transcription Factor Required for Immunity to Bacterial and Fungal Pathogens

PLoS ONE ◽  
2006 ◽  
Vol 1 (1) ◽  
pp. e77 ◽  
Author(s):  
Samantha Kerry ◽  
Michael TeKippe ◽  
Nathan C. Gaddis ◽  
Alejandro Aballay
Keyword(s):  
Transcription Factor ◽  
Fungal Pathogens ◽  
Gata Transcription Factor

scholarly journals Nonhost Resistance of Arabidopsis thaliana Against Alternaria alternata Involves both Pre- and Postinvasive Defenses but Is Collapsed by AAL-Toxin in the Absence of LOH2

2013 ◽  
Vol 103 (7) ◽  
pp. 733-740 ◽  
Author(s):  
Mayumi Egusa ◽  
Takuya Miwa ◽  
Hironori Kaminaka ◽  
Yoshitaka Takano ◽  
Motoichiro Kodama
Keyword(s):  
Arabidopsis Thaliana ◽  
Alternaria Alternata ◽  
Defense Mechanisms ◽  
Stem Canker ◽  
Hypersensitive Reaction ◽  
Nonhost Resistance ◽  
Necrotrophic Pathogen ◽  
Toxin Resistance ◽  
Tomato Pathotype ◽  
Aal Toxin

The tomato pathotype of Alternaria alternata causes Alternaria stem canker on tomato depending upon the production of the host-specific AAL-toxin. Host defense mechanisms to A. alternata, however, are largely unknown. Here, we elucidate some of the mechanisms of nonhost resistance to A. alternata using Arabidopsis mutants. Wild-type Arabidopsis showed either no symptoms or a hypersensitive reaction (HR) when inoculated with both strains of AAL-toxin-producing and non-producing A. alternata. Yet, when these Arabidopsis penetration (pen) mutants, pen2 and pen3, were challenged with both strains of A. alternata, fungal penetration was possible. However, further fungal development and conidiation were limited on these pen mutants by postinvasion defense with HR-like cell death. Meanwhile, only AAL-toxin-producing A. alternata could invade lag one homologue (loh)2 mutants, which have a defect in the AAL-toxin resistance gene, subsequently allowing the fungus to complete its life cycle. Thus, the nonhost resistance of Arabidopsis thaliana to A. alternata consists of multilayered defense systems that include pre-invasion resistance via PEN2 and PEN3 and postinvasion resistance. However, our study also indicates that the pathogen is able to completely overcome the multilayered nonhost resistance if the plant is sensitive to the AAL-toxin, which is an effector of the toxin-dependent necrotrophic pathogen A. alternata.

scholarly journals The Role of IL-33 in Host Response toCandida albicans

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
C. Rodríguez-Cerdeira ◽  
A. Lopez-Bárcenas ◽  
B. Sánchez-Blanco ◽  
R. Arenas
Keyword(s):  
Defense Mechanisms ◽  
Fungal Pathogens ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Case Reports ◽  
Pathogenic Fungi ◽  
Cell Types ◽  
Immune Defense ◽  
Beneficial Role

Background. Interleukin (IL) 33 is a recently identified pleiotropic cytokine that influences the activity of multiple cell types and orchestrates complex innate and adaptive immune responses.Methods. We performed an extensive review of the literature published between 2005 and 2013 on IL-33 and related cytokines, their functions, and their regulation of the immune system followingCandida albicanscolonization. Our literature review included cross-references from retrieved articles and specific data from our own studies.Results. IL-33 (IL-1F11) is a recently identified member of the IL-1 family of cytokines. Accumulating evidence suggests a pivotal role of the IL-33/ST2 axis in host immune defense against fungal pathogens, includingC. albicans. IL-33 induces a Th2-type inflammatory response and activates both innate and adaptive immunity. Studies in animal models have shown that Th2 inflammatory responses have a beneficial role in immunity against gastrointestinal and systemic infections byCandidaspp.Conclusions. This review summarizes the most important clinical studies and case reports describing the beneficial role of IL-33 in immunity and host defense mechanisms against pathogenic fungi. The finding that the IL-33/ST2 axis is involved in therapeutic target has implications for the prevention and treatment of inflammatory diseases, including acute or chronic candidiasis.

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