Microbial assemblies associated with temperature sensitivity of soil respiration along an altitudinal gradient

10 páginas.. 4 figuras.- referencias.- Supplementary data to this article can be found online at https://doi. org/10.1016/j.scitotenv.2022.153257Identifying the drivers of the response of soil microbial respiration to warming is integral to accurately forecasting the carbon-climate feedbacks in terrestrial ecosystems. Microorganisms are the fundamental drivers of soil microbial respiration and its response to warming; however, the specific microbial communities and properties involved in the process remain largely undetermined. Here, we identified the associations between microbial community and temperature sensitivity (Q10) of soil microbial respiration in alpine forests along an altitudinal gradient (from 2974 to 3558 m) from the climate-sensitive Tibetan Plateau. Our results showed that changes in microbial community composition accounted for more variations of Q10 values than a wide range of other factors, including soil pH, moisture, substrate quantity and quality, microbial biomass, diversity and enzyme activities. Specifically, co-occurring microbial assemblies (i.e., ecological clusters or modules) targeting labile carbon consumption were negatively correlated with Q10 of soil microbial respiration, whereas microbial assemblies associated with recalcitrant carbon decomposition were positively correlated with Q10 of soil microbial respiration. Furthermore, there were progressive shifts of microbial assemblies from labile to recalcitrant carbon consumption along the altitudinal gradient, supporting relatively high Q10 values in high-altitude regions. Our results provide new insights into the link between changes in major microbial assemblies with different trophic strategies and Q10 of soil microbial respiration along an altitudinal gradient, highlighting that warming could have stronger effects on microbially-mediated soil organic matter decomposition in high-altitude regions than previously thought.This research was supported by the National Natural Science Foundation of China (32071595 and 41830756). We also thank the Fundamental Research Funds for the Central Universities (Program no. 2662019PY010 and 2662019QD055), Natural Science Fund of Hubei Province (2019CFA094), and the Strategic Priority Research Program (A) of the Chinese Academy of Sciences (Grant No. XDA20040502). We thank Hailong Li for his assistance in field sampling, and Jinhuang Lin for mapping sample locations. M.D-B. is supported by a Ramón y Cajal grant from the Spanish Government (agreement no. RYC2018-025483-I). ReferencesPeer reviewe

CPT1A mediates chemoresistance in human hypopharyngeal squamous cell carcinoma via ATG16L1-dependent cellular autophagy

Hypopharyngeal squamous cell carcinoma (HSCC) is a highly aggressive malignancy that constitutes approximately 95% of all hypopharyngeal carcinomas, and it carries a poor prognosis. The primary factor influencing the efficacy of anti-cancer drugs for this type of carcinoma is chemoresistance. Carnitine palmitoyltransferase 1A (CPT1A) has been associated with tumor progression in various cancers, including breast, gastric, lung, and prostate cancer. The inhibition or depletion of CPT1A can lead to apoptosis, curbing cancer cell proliferation and chemoresistance. However, the role of CPT1A in HSCC is not yet fully understood. In this study, we discovered that CPT1A is highly expressed in HSCC and is associated with an advanced T-stage and a poor 5-year survival rate among patients. Furthermore, the overexpression of CPT1A contributes to HSCC chemoresistance. Mechanistically, CPT1A can interact with the autophagy-related protein ATG16L1 and stimulate the succinylation of ATG16L1, which in turn drives autophagosome formation and autophagy. We also found that treatment with 3-methyladenine (3-MA) can reduce cisplatin resistance in HSCC cells that overexpress CPT1A. Our findings also showed that a CPT1A inhibitor significantly enhances cisplatin sensitivity both in vitro and in vivo. This study is the first to suggest that CPT1A has a regulatory role in autophagy and is linked to poor prognosis in HSCC patients. It presents novel insights into the roles of CPT1A in tumorigenesis and proposes that CPT1A could be a potential therapeutic target for HSCC treatment