Pathogenicity Variation in Two Genomes of Cercospora Species Causing Gray Leaf Spot in Maize.

The gray leaf spots caused by Cercospora spp. severely affect the yield and quality of maize. However, the evolutionary relation and pathogenicity variation between species of the Cercospora genus is largely unknown. In this study, we constructed high-quality reference genomes by nanopore sequencing two Cercospora species, namely, C. zeae-maydis and C. zeina, with differing pathogenicity, collected from northeast (Liaoning [LN]) and southeast (Yunnan [YN]) China, respectively. The genome size of C. zeae-maydis-LN is 45.08 Mb, containing 10,839 annotated genes, whereas that of Cercospora zeina-YN is 42.18 Mb, containing 10,867 annotated genes, of which approximately 86.58% are common in the two species. The difference in their genome size is largely attributed to increased long terminal repeat retrotransposons of 3.8 Mb in total length in C. zeae-maydis-LN. There are 41 and 30 carbohydrate-binding gene subfamilies identified in C. zeae-maydis-LN and C. zeina-YN, respectively. A higher number of carbohydrate-binding families found in C. zeae-maydis-LN, and its unique CBM4, CBM37, and CBM66, in particular, may contribute to variation in pathogenicity between the two species, as the carbohydrate-binding genes are known to encode cell wall-degrading enzymes. Moreover, there are 114 and 107 effectors predicted, with 47 and 46 having unique potential pathogenicity in C. zeae-maydis-LN and C. zeina-YN, respectively. Of eight effectors randomly selected for pathogenic testing, five were found to inhibit cell apoptosis induced by Bcl-2-associated X. Taken together, our results provide genomic insights into variation in pathogenicity between C. zeae-maydis and C. zeina. [Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Capsaicin inhibits glycolysis in esophageal squamous cell carcinoma by regulating hexokinase­2 expression.

Capsaicin is a principal component of hot red peppers and chili peppers. Previous studies have reported that capsaicin exhibits antitumor functions in a variety of tumor models. Although various mechanisms underlying the capsaicin­mediated inhibition of tumor growth have been demonstrated, the impact of capsaicin on tumor metabolism has rarely been reported. The present study demonstrated that capsaicin exhibited an inhibitory effect on tumor glycolysis in esophageal squamous cell carcinoma (ESCC) cells. Following treatment with capsaicin, glucose consumption and lactate production in ESCC cells was decreased. Capsaicin resulted in a decrease of hexokinase­2 (HK­2) expression, which is known for its important role in tumor glycolysis. Further investigations demonstrated that phosphatase and tensin homolog (PTEN) expression was increased in ESCC cells treated with capsaicin, and that the RAC­α serine threonine­protein kinase signaling pathway was downregulated. In PTEN­knockdown KYSE150 cells, the decrease in HK­2 and inhibition of glycolysis caused by capsaicin was attenuated, which suggested that the impact of capsaicin on tumor metabolism was associated with its effect on PTEN.