Dissection of genetic architecture of nine hazardous component traits of mainstream smoke in tobacco (Nicotiana tabacum L.).

Tobacco (Nicotiana tabacum L.) use is the leading cause of preventable death, due to deleterious chemical components and smoke from tobacco products, and therefore reducing harmful chemical components in tobacco is one of the crucial tobacco breeding targets. However, due to complexity of tobacco smoke and unavailability of high-density genetic maps, the genetic architecture of representative hazardous smoke has not been fully dissected. The present study aimed to explore the genetic architecture of nine hazardous component traits of mainstream smoke through QTL mapping using 271 recombinant inbred lines (RILs) derived from K326 and Y3 in multiple environments. The analysis of genotype and genotype by environment interaction (GE) revealed substantially greater heritability over 95% contributed mostly by GE interaction effects. We also observed strong genetic correlations among most studied hazardous smoke traits, with the highest correlation coefficient of 0.84 between carbon monoxide and crotonaldehyde. Based on a published high-density genetic map, a total of 19 novel QTLs were detected for eight traits using a full QTL model, of which 17 QTLs showed significant additive effects, six showed significant additive-by-environment interaction effects, and one pair showed significant epistasis-by-environment interaction effect. Bioinformatics analysis of sequence in QTL region predicted six genes as candidates for four traits, of which Nt21g04598.1, Nt21g04600.1, and Nt21g04601.1 had pleiotropic effects on PHE and TAR.

Honokiol attenuates acetaminophen-induced acute liver injury by inhibiting hepatic CYP1A2 activity and improving liver mitochondrial dysfunction.

Objective: Acetaminophen (APAP) overdose is a common cause of liver injury. This study aimed to investigate the protective effect of honokiol (Hon) against APAP-induced hepatotoxicity and its potential mechanism. Methods: C57BL/6 mice were administrated with Hon (10 and 30 mg/kg) after APAP (300 mg/kg) treatment. On 1.5 h and 5 h after Hon treatment, mice were sacrificed. Serum and liver were collected. And then, liver injury-related indexes, APAP metabolism-related indexes, mitochondrial respiratory chain function-related indexes, and mitochondrial membrane function-related protein expression were evaluated. Results: It was found that Hon significantly decreased serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) activity and glutathione (GSH) depletion, increased hepatic catalase (CAT) and GSH peroxidase (GSH-Px) activities, reduced hepatic MDA and 3-nitrotyrosine contents, inhibited hepatic CYP1A2 activity and APAP protein adducts (APAP-CYS) formation. Meanwhile, oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV in mitochondrial respiratory chain was increased, whereas the release of H2O2 in the mitochondria was decreased following Hon treatment. Furthermore, Hon markedly down-regulated p-JNK in both cytosol and mitochondria, and obviously inhibited the release of apoptosis inducing factor (AIF) and endonuclease G (EndoG) from mitochondria to cytosol. Conclusion: Hon alleviated APAP-induced liver injury through the following pathways: Reducing the production of APAP-CYS by inhibiting CYP1A2 activity; Ameliorating hepatic oxidative stress by increasing the levels of hepatic CAT, GSH-Px and GSH; Improving mitochondrial respiratory chain function by promoting oxidative phosphorylation capacity of complex I and electron transfer capacity of complex IV; Improving the function of mitochondrial membrane by inhibiting p-JNK and its translocation to mitochondria, thereby reducing the release of AIF and EndoG.

The transcriptional reprograming and functional identification of WRKY family members in pepper's response to Phytophthora capsici infection.

BACKGROUND: Plant transcription factors (TFs) are key transcriptional regulators to manipulate the regulatory network of host immunity. However, the globally transcriptional reprogramming of plant TF families in response to pathogens, especially between the resistant and susceptible host plants, remains largely unknown. RESULTS: Here, we performed time-series RNA-seq from a resistant pepper line CM334 and a susceptible pepper line EC01 upon challenged with Phytophthora capsici, and enrichment analysis indicated that WRKY family most significantly enriched in both CM334 and EC01. Interestingly, we found that nearly half of the WRKY family members were significantly up-regulated, whereas none of them were down-regulated in the two lines. These induced WRKY genes were greatly overlapped between CM334 and EC01. More strikingly, most of these induced WRKY genes were expressed in time-order patterns, and could be mainly divided into three subgroups: early response (3 h-up), mid response (24 h-up) and mid-late response (ML-up) genes. Moreover, it was found that the responses of these ML-up genes were several hours delayed in EC01. Furthermore, a total of 19 induced WRKY genes were selected for functional identification by virus-induced gene silencing. The result revealed that silencing of CaWRKY03-6, CaWRKY03-7, CaWRKY06-5 or CaWRKY10-4 significantly increase the susceptibility to P. capsici both in CM334 and EC01, indicating that they might contribute to pepper's basal defense against P. capsici; while silencing of CaWRKY08-4 and CaWRKY01-10 significantly impaired the disease resistance in CM334 but not in EC01, suggesting that these two WRKY genes are prominent modulators specifically in the resistant pepper plants. CONCLUSIONS: These results considerably extend our understanding of WRKY gene family in pepper's resistance against P. capsici and provide potential applications for genetic improvement against phytophthora blight.