scholarly journals MdWRKY75e enhances resistance to Alternaria alternata in Malus domestica

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Yingjun Hou ◽  
Xinyi Yu ◽  
Weiping Chen ◽  
Weibing Zhuang ◽  
Sanhong Wang ◽  
...  

AbstractThe Alternaria alternata apple pathotype adversely affects apple (Malus domestica Borkh.) cultivation. However, the molecular mechanisms underlying enhanced resistance to this pathogen in apple remain poorly understood. We have previously reported that MdWRKY75 expression is upregulated by A. alternata infection in ‘Sushuai’ apples. In this study, we discovered that overexpression of MdWRKY75e increased the resistance of transgenic apple lines to A. alternata infection, whereas silencing this gene enhanced susceptibility to A. alternata infection. Furthermore, we found that MdWRKY75e directly binds to the MdLAC7 promoter to regulate the biosynthesis of laccase and increase the biosynthesis of lignin during A. alternata infection. Moreover, the thickening of the cell wall enhanced the mechanical defense capabilities of apple. In addition, we found that jasmonic acid remarkably induced MdWRKY75e expression, and its levels in transgenic apple lines were elevated. These results indicate that MdWRKY75e confers resistance to the A. alternata apple pathotype mainly via the jasmonic acid pathway and that pathogenesis-related genes and antioxidant-related enzyme activity are involved in the disease resistance of MdWRKY75e transgenic plants. In conclusion, our findings provide insights into the importance of MdWRKY75e for resistance to A. alternata infection in apples.

2021 ◽  
Vol 22 (11) ◽  
pp. 5713
Author(s):  
Yiping Zhang ◽  
Li Zhang ◽  
Hai Ma ◽  
Yichu Zhang ◽  
Xiuming Zhang ◽  
...  

APETALA2/ETHYLENE RESPONSIVE FACTOR (AP2/ERF) transcription factors play important roles in plant development and stress response. Although AP2/ERF genes have been extensively investigated in model plants such as Arabidopsis thaliana, little is known about their role in biotic stress response in perennial fruit tree crops such as apple (Malus × domestica). Here, we investigated the role of MdERF100 in powdery mildew resistance in apple. MdERF100 localized to the nucleus but showed no transcriptional activation activity. The heterologous expression of MdERF100 in Arabidopsis not only enhanced powdery mildew resistance but also increased reactive oxygen species (ROS) accumulation and cell death. Furthermore, MdERF100-overexpressing Arabidopsis plants exhibited differential expressions of genes involved in jasmonic acid (JA) and salicylic acid (SA) signaling when infected with the powdery mildew pathogen. Additionally, yeast two-hybrid and bimolecular fluorescence complementation assays confirmed that MdERF100 physically interacts with the basic helix–loop–helix (bHLH) protein MdbHLH92. These results suggest that MdERF100 mediates powdery mildew resistance by regulating the JA and SA signaling pathways, and MdbHLH92 is involved in plant defense against powdery mildew. Overall, this study enhances our understanding of the role of MdERF genes in disease resistance, and provides novel insights into the molecular mechanisms of powdery mildew resistance in apple.


2007 ◽  
Vol 97 (7) ◽  
pp. 794-802 ◽  
Author(s):  
Shobha D. Potlakayala ◽  
Darwin W. Reed ◽  
Patrick S. Covello ◽  
Pierre R. Fobert

Systemic acquired resistance (SAR) is an induced defense response that confers long-lasting protection against a broad range of microbial pathogens. Here we show that treatment of Brassica napus plants with the SAR-inducing chemical benzo-(1,2,3)-thiadiazole-7-carbothioic acid S-methyl ester (BTH) significantly enhanced resistance against virulent strains of the bacterial pathogen Pseudomonas syringae pv. maculicola and the fungal pathogen Leptosphaeria maculans. Localized preinoculation of plants with an avirulent strain of P. syringae pv. maculicola also enhanced resistance to these pathogens but was not as effective as BTH treatment. Single applications of either SAR-inducing pretreatment were effective against P. syringae pv. maculicola, even when given more than 3 weeks prior to the secondary challenge. The pretreatments also led to the accumulation of pathogenesis-related (PR) genes, including BnPR-1 and BnPR-2, with higher levels of transcripts observed in the BTH-treatment material. B. napus plants expressing a bacterial salicylate hydroxylase transgene (NahG) that metabolizes salicylic acid to catechol were substantially compromised in SAR and accumulated reduced levels of PR gene transcripts when compared with untransformed controls. Thus, SAR in B. napus displays many of the hallmarks of classical SAR including long lasting and broad host range resistance, association with PR gene activation, and a requirement for salicylic acid.


2016 ◽  
Vol 29 (4) ◽  
pp. 562-571 ◽  
Author(s):  
Chethan Gejjalagere Honnappa ◽  
Unnikrishnan Mazhuvancherry Kesavan

Inflammatory diseases are complex, multi-factorial outcomes of evolutionarily conserved tissue repair processes. For decades, non-steroidal anti-inflammatory drugs and cyclooxygenase inhibitors, the primary drugs of choice for the management of inflammatory diseases, addressed individual targets in the arachidonic acid pathway. Unsatisfactory safety and efficacy profiles of the above have necessitated the development of multi-target agents to treat complex inflammatory diseases. Current anti-inflammatory therapies still fall short of clinical needs and the clinical trial results of multi-target therapeutics are anticipated. Additionally, new drug targets are emerging with improved understanding of molecular mechanisms controlling the pathophysiology of inflammation. This review presents an outline of small molecules and drug targets in anti-inflammatory therapeutics with a summary of a newly identified target AMP-activated protein kinase, which constitutes a novel therapeutic pathway in inflammatory pathology.


2021 ◽  
Vol 12 ◽  
Author(s):  
Alongkorn Kurilung ◽  
Vincent Perreten ◽  
Nuvee Prapasarakul

Leptospira weilii belongs to the pathogenic Leptospira group and is a causal agent of human and animal leptospirosis in many world regions. L. weilii can produce varied clinical presentations from asymptomatic through acute to chronic infections and occupy several ecological niches. Nevertheless, the genomic feature and genetic basis behind the host adaptability of L. weilii remain elusive due to limited information. Therefore, this study aimed to examine the complete circular genomes of two new L. weilii serogroup Mini strains (CUDO6 and CUD13) recovered from the urine of asymptomatic dogs in Thailand and then compared with the 17 genomes available for L. weilii. Variant calling analysis (VCA) was also undertaken to gain potential insight into the missense mutations, focusing on the known pathogenesis-related genes. Whole genome sequences revealed that the CUDO6 and CUD13 strains each contained two chromosomes and one plasmid, with average genome size and G+C content of 4.37 Mbp and 40.7%, respectively. Both strains harbored almost all the confirmed pathogenesis-related genes in Leptospira. Two novel plasmid sequences, pDO6 and pD13, were identified in the strains CUDO6 and CUD13. Both plasmids contained genes responsible for stress response that may play important roles in bacterial adaptation during persistence in the kidneys. The core-single nucleotide polymorphisms phylogeny demonstrated that both strains had a close genetic relationship. Amongst the 19 L. weilii strains analyzed, the pan-genome analysis showed an open pan-genome structure, correlated with their high genetic diversity. VCA identified missense mutations in genes involved in endoflagella, lipopolysaccharide (LPS) structure, mammalian cell entry protein, and hemolytic activities, and may be associated with host-adaptation in the strains. Missense mutations of the endoflagella genes of CUDO6 and CUD13 were associated with loss of motility. These findings extend the knowledge about the pathogenic molecular mechanisms and genomic evolution of this important zoonotic pathogen.


2019 ◽  
Author(s):  
Nicholas Gladman ◽  
Yinping Jiao ◽  
Young Koung Lee ◽  
Lifang Zhang ◽  
Ratan Chopra ◽  
...  

AbstractAs in other cereal crops, the panicles of sorghum (Sorghum bicolor (L.) Moench) comprise two types of floral spikelets (grass flowers). Only sessile spikelets (SSs) are capable of producing viable grains, whereas pedicellate spikelets (PSs) cease development after initiation and eventually abort. Consequently, grain number per panicle (GNP) is lower than the total number of flowers produced per panicle. The mechanism underlying this differential fertility is not well understood. To investigate this issue, we isolated a series of EMS-induced multiseeded (msd) mutants that result in full spikelet fertility, effectively doubling GNP. Previously, we showed that MSD1 is a TCP (Teosinte branched/Cycloidea/PCF) transcription factor that regulates jasmonic acid (JA) biosynthesis, and ultimately floral sex organ development. Here, we show that MSD2 encodes a lipoxygenase (LOX) that catalyzes the first committed step of JA biosynthesis. Further, we demonstrate that MSD1 binds to the promoters of MSD2 and other JA pathway genes. Together, these results show that a JA-induced module regulates sorghum panicle development and spikelet fertility. The findings advance our understanding of inflorescence development and could lead to new strategies for increasing GNP and grain yield in sorghum and other cereal crops.SignificanceThrough a single base pair mutation, grain number can be increased by ~200% in the globally important crop Sorghum bicolor. This mutation affects the expression of an enzyme, MSD2, that catalyzes the jasmonic acid pathway in developing floral meristems. The global gene expression profile in this enzymatic mutant is similar to that of a transcription factor mutant, msd1, indicating that disturbing any component of this regulatory module disrupts a positive feedback loop that occurs normally due to regular developmental perception of jasmonic acid. Additionally, the MSD1 transcription factor is able to regulate MSD2 in addition to other jasmonic acid pathway genes, suggesting that it is a primary transcriptional regulator of this hormone signaling pathway in floral meristems.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jie Sheng ◽  
Nick K. Olrichs ◽  
Willie J. Geerts ◽  
Dora V. Kaloyanova ◽  
J. Bernd Helms

Abstract Members of the CAP superfamily (Cysteine-rich secretory proteins, Antigen 5, and Pathogenesis-Related 1 proteins) are characterized by the presence of a structurally conserved CAP domain. The common structure-function relationship of this domain is still poorly understood. In this study, we unravel specific molecular mechanisms modulating the quaternary structure of the mammalian CAP protein GAPR-1 (Golgi-Associated plant Pathogenesis-Related protein 1). Copper ions are shown to induce a distinct amyloid-like aggregation pathway of GAPR-1 in the presence of heparin. This involves an immediate shift from native multimers to monomers which are prone to form amyloid-like fibrils. The Cu2+-induced aggregation pathway is independent of a conserved metal-binding site and involves the formation of disulfide bonds during the nucleation process. The elongation process occurs independently of the presence of Cu2+ ions, and amyloid-like aggregation can proceed under oxidative conditions. In contrast, the Zn2+-dependent aggregation pathway was found to be independent of cysteines and was reversible upon removal of Zn2+ ions. Together, our results provide insight into the regulation of the quaternary structure of GAPR-1 by metal ions and redox homeostasis with potential implications for regulatory mechanisms of other CAP proteins.


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