, one of the most detrimental necrotrophic pathogens, causes rice sheath blight and poses a severe threat to production. Focus on the function of effectors secreted by necrotrophic pathogens during infection has grown rapidly in recent years. However, little is known about the virulence and mechanisms of these proteins. In this study, we performed functional studies on putative effectors in and revealed that AGLIP1 out of 13 putative effectors induced cell death in . AGLIP1 was also demonstrated to trigger cell death in rice protoplasts. The predicted lipase active sites and signal peptide (SP) of this protein were required for the cell death-inducing ability. was greatly induced during infection in rice sheath. The AGLIP1's virulence function was further demonstrated by transgenic technology. The pathogenesis-related genes induced by pathogen-associated molecular pattern and bacteria were remarkably inhibited in AGLIP1-expressing transgenic lines. Ectopic expression of AGLIP1 strongly facilitated disease progression in caused by the type III secretion system-defective mutant from pv. tomato DC3000. Collectively, these results indicate that AGLIP1 is a possible effector that plays a significant role in pathogen virulence through inhibiting basal defenses and promoting disease development in plants.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6775501PMC
http://dx.doi.org/10.3389/fmicb.2019.02228DOI Listing

Publication Analysis

Top Keywords

cell death
12
disease development
8
necrotrophic pathogens
8
rice sheath
8
putative effectors
8
effector aglip1
4
aglip1 ag1
4
ag1 triggers
4
cell
4
triggers cell
4

Similar Publications

Avian pathogenic Escherichia coli (APEC) is a significant pathogen infecting poultry that is responsible for high mortality, morbidity and severe economic losses to the poultry industry globally, posing a substantial risk to the health of poultry. APEC encounters reactive oxygen species (ROS) during the infection process and thus has evolved antioxidant defense mechanisms to protect against oxidative damage. The imbalance of ROS production and antioxidant defenses is known as oxidative stress, which results in oxidative damage to proteins, lipids and DNA, and even bacterial cell death.

View Article and Find Full Text PDF

Microglia-like cells from patient monocytes demonstrate increased phagocytic activity in probable Alzheimer's disease.

Mol Cell Neurosci

December 2024

Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Türkiye; Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Türkiye; Department of Neuroscience, Institute of Health Sciences, Dokuz Eylul University, Izmir, Türkiye. Electronic address:

Alzheimer's disease (AD) is a neurodegenerative disorder that is characterized by the accumulation of amyloid plaques, phosphorylated tau tangles and microglia toxicity, resulting in neuronal death and cognitive decline. Since microglia are recognized as one of the key players in the disease, it is crucial to understand how microglia operate in disease conditions and incorporate them into models. The studies on human microglia functions are thought to reflect the post-symptomatic stage of the disease.

View Article and Find Full Text PDF

Self-assembled natural triterpenoids for the delivery of cyclin-dependent kinase 4/6 inhibitors to enhance cancer chemoimmunotherapy.

J Control Release

December 2024

Key Laboratory of Natural Medicine Innovation and Transformation, Henan University, Kaifeng 475000, PR China; State Key Laboratory of Antiviral Drugs, Henan University, Kaifeng 475000, PR China; Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100050, PR China. Electronic address:

Immunogenic cell death (ICD) has recently emerged as a promising strategy in reinforcing anti-PD-L1 blockade immunotherapy of triple-negative breast cancer (TNBC). The CDK4/6 inhibitor palbociclib (PAL), as a clinical star medicine targeting the cell cycle machinery, is an ideal candidate for fabricating a highly efficient ICD inducer for TNBC chemoimmunotherapy. However, the frequently observed chemoresistance and clinical adverse effects, as well as significant antagonistic effects when co-administered with certain chemotherapeutics, have seriously restricted the efficiency of PAL and the feasibility of combination strategies.

View Article and Find Full Text PDF

Background & Aims: Metabolic dysfunction-associated steatotic liver (MASLD) progression is driven by chronic inflammation and fibrosis, largely influenced by Kupffer cell (KC) dynamics, particularly replenishment of pro-inflammatory monocyte-derived KCs (MoKCs) due to increased death of embryo-derived KCs. Adenosine A3 receptor (A3AR) plays a key role in regulating metabolism and immune responses, making it a promising therapeutic target. This study aimed to investigate the impact of selective A3AR antagonism for regulation of replenished MoKCs, thereby improving MASLD.

View Article and Find Full Text PDF

Loss-of-function SLC25A20 mutation causes carnitine-acylcarnitine translocase deficiency by reducing SLC25A20 protein stability.

Gene

December 2024

Department of Medical Genetics/Experimental Education/Administration Center, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Single Cell Technology and Application, Guangzhou 510515, China; Department of Fetal Medicine and Prenatal Diagnosis, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China. Electronic address:

Background/aim: Autosomal-recessive carnitine-acylcarnitine translocase deficiency (CACTD) is a rare disorder of long-chain fatty acid oxidation caused by variants in the SLC25A20 gene. Under fasting conditions, most newborns with severe CACTD experience sudden cardiac arrest and hypotonia, often leading to premature death due to rapid disease progression. Understanding of genetic factors and pathogenic mechanisms in CACTD is essential for its diagnosis, treatment, and prevention.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!