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Yee, K.

Publications and source records attributed to Yee, K..

2 recordsLinked to original sources

SPRAY-INDUCED GENE SILENCING IDENTIFIES PATHOGEN PROCESSES CONTRIBUTING TO POWDERY MILDEW PROLIFERATION

Spray-induced gene silencing (SIGS) is an emerging tool for crop pest protection. It utilizes exogenously applied double stranded RNA to specifically reduce pest target gene expression using endogenous RNA interference machinery. Powdery mildews, widespread obligate biotrophic fungi infect agricultural crops including wheat, barley, cucurbits, grapevine, and ornamentals such as roses. In this study, SIGS methods were developed and optimized for powdery mildews using the known azole-fungicide target CYP51 and the Golovinomyces orontii-Arabidopsis thaliana pathosystem. Additional screening resulted in the identification of conserved gene targets and processes important to powdery mildew proliferation: apoptosis-antagonizing transcription factor in essential cellular metabolism and stress response; lipase a, lipase 1, and acetyl-CoA oxidase in lipid catabolism; 9-cis-epoxycarotenoid dioxygenase, xanthoxin dehydrogenase, and a putative abscisic acid G-protein coupled receptor predicted to function in manipulation of the plant hormone abscisic acid; and the secreted effector EC2. Powdery mildew is the dominant disease impacting grapes and extensive powdery mildew resistance to applied fungicides has been reported. Therefore, we developed SIGS for the Erysiphe necator-Vitis vinifera system and tested six successful targets identified using the G. orontii-A. thaliana system. For all targets tested, a similar reduction in powdery mildew disease was observed between systems. This indicates screening of broadly conserved targets in the G. orontii-A. thaliana pathosystem identifies targets and processes for the successful control of other powdery mildews. The flexibility, specificity, reduced environmental and health risks, and rapid transition from the bench to the field make SIGS an exciting prospect for commercial powdery mildew control.

microbiology↗

TET1 controls Cxcl1 induction by DNA demethylation and promotes neutrophil recruitment during acute lung injury

Neutrophils are rapidly recruited from the peripheral blood to the inflammatory site to initiate inflammatory response against pathogenic infections. The process to recruit neutrophils must be properly regulated since the abnormal accumulation of neutrophils can cause organ damage and dysfunction. The acute respiratory distress syndrome (ARDS)/acute lung injury (ALI) is a common cause of respiratory failure that is characterized by the infiltration of neutrophils and epithelial integrity disruption. Indeed, recent studies suggest a pathogenic role of neutrophils in the clinic severity of the coronavirus disease 2019 (COVID-19) ARDS. The chemokine CXCL1, which is rapidly induced by inflammatory stimuli, plays a key role in neutrophil influx during lung inflammation. The molecular basis of Cxcl1 induction is not fully understood. Here we report that TET1, a member of the ten eleven translocation (TET) methylcytosine dioxygenase protein family, displays a striking specificity in the regulation of gene expression in macrophages. RNA sequencing (RNA-seq) analysis showed that Tet1 disruption significantly altered the expression of only 48 genes that include Cxcl1 and several other genes known to be important for cell migration and trafficking in bone marrow derived macrophages (BMDMs) in response to LPS stimulation. TET1 regulates the induction of Cxcl1 by facilitating the DNA demethylation of the Cxcl1 promoter. In Tet1-/- mice, the induction of Cxcl1 was suppressed, resulting in defective neutrophil recruitment to the lung during LPS-induced acute lung injury. Our results identify a novel epigenetic mechanism that selectively controls Cxcl1 induction and neutrophil recruitment during acute lung injury. Key PointsO_LITET1 has a striking specificity in macrophage gene regulation and controls Cxcl1 induction by inflammatory stimuli via DNA demethylation C_LIO_LINeutrophil recruitment is defective in Tet1 deficient mice during acute lung injury C_LI

immunology↗