Dehydrin-Like Proteins in Soybean Seeds in Response to Drought Stress during Seed Filling

There is no information on accumulation of dehydrin proteins during seed development and maturation of soybean [Glycine max (L.) Merr.] in response to drought stress. Our objective was to study accumulation of dehydrin-like proteins in developing soybean seeds in response to drought stress. A greenhouse experiment and a field experiment were conducted. In the greenhouse experiment, three treatments were imposed on soybean plants after beginning of linear seed filling (R5): well-watered (WW), gradual stress (GS) imposed before severe stress, and sudden severe stress (SS). In the field treatments were irrigation (I) and nonirrigation (NI) (rainfed) conditions imposed from R5 to R8 (mature seeds). Greenhouse results indicated dehydrin-like proteins (28 and 32 kDa) were detected 18 d after R5 (R5.8) in developing seeds from drought-stressed plants but not in seeds from the well-watered plants. In the mature seeds, dehydrin-like proteins (28, 32, and 34 kDa) were detected in seeds from drought-stressed plants as well as the well-watered plants. In the field, dehydrin-like proteins accumulated similarly under irrigation and nonirrigation conditions, with the first detection for dehydrins (28 and 32 kDa) at 22 d after R5 (R6). Accumulation of dehydrin-like proteins was maximal in seeds harvested at 43 d after R5 (seed physiological maturity)

SIRT1-NOX4 Signaling Axis Regulates Cancer Cachexia

Approximately one third of cancer patients die due to complexities related to cachexia. However, the mechanisms of cachexia and the potential therapeutic interventions remain poorly studied. We observed a significant positive correlation between SIRT1 expression and muscle fiber cross-sectional area in pancreatic cancer patients. Rescuing Sirt1 expression by exogenous expression or pharmacological agents reverted cancer cell-induced myotube wasting in culture conditions and mouse models. RNA-seq and follow-up analyses showed cancer cell-mediated SIRT1 loss induced NF-κB signaling in cachectic muscles that enhanced the expression of FOXO transcription factors and NADPH oxidase 4 (Nox4), a key regulator of reactive oxygen species production. Additionally, we observed a negative correlation between NOX4 expression and skeletal muscle fiber cross-sectional area in pancreatic cancer patients. Knocking out Nox4 in skeletal muscles or pharmacological blockade of Nox4 activity abrogated tumor-induced cachexia in mice. Thus, we conclude that targeting the Sirt1-Nox4 axis in muscles is an effective therapeutic intervention for mitigating pancreatic cancer-induced cachexia