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Zhuang, G.

Publications and source records attributed to Zhuang, G..

2 recordsLinked to original sources

In-House Forecasting of Crop Latitude Adaptation through a Daylength-sensing-based Environment Adaptation Simulator (DEAS)

Global climate change necessitates the accelerated breeding of new crop varieties that can sustain yields in new environments. As a proxy for environmental adaptation, the selection of crops that can adapt to different latitudes is an appealing strategy. However, such selection currently involves a lengthy procedure that severely restricts the rapid breeding of varieties. Here, we aimed to combine molecular technologies with an in-house streamlined screening method to facilitate rapid selection for latitude adaptation. We established the Daylength-sensing-based Environment Adaptation Simulator (DEAS) to measure crop latitude adaptation via the transcriptional dynamics of florigen genes at different latitudes. We used different statistical approaches to demonstrate that DEAS predicts the florigen expression profiles in rice with high accuracy. Furthermore, we demonstrated the potential for application of DEAS in different crops. Incorporating DEAS into the breeding programs of conventional and underutilized crops could help meet the future needs for crop adaptation and promote sustainable agriculture.

plant biology↗

Loss of SHMT2 mediates 5-FU chemoresistance by inducing autophagy in colorectal cancer

Serine hydroxymethyltransferase 2 (SHMT2) plays a vital role in one-carbon metabolism and drives colorectal carcinogenesis. In our study, loss of SHMT2 induced 5-Fluorouracil (5-FU) chemoresistance and was associated with poor prognosis in colorectal cancer (CRC). To elucidate the possible mechanism and generate a strategy to sensitize CRC to 5-FU chemotherapy, we first identified the binding proteins of SHMT2 in cancer cells by mass spectrometry. We found that SHMT2 inhibited autophagy through binding cytoplasmic p53. In fact, SHMT2 prevented cytoplasmic p53 degradation by inhibiting the binding of p53 and HDM2. Under treatment with 5-FU, depletion of SHMT2 promoted autophagy and inhibited apoptosis. Autophagy inhibitors CQ decreased low SHMT2-induced 5-FU resistance in vitro and in vivo. Finally, we enhanced the lethality of 5-FU treatment to CRC cells through the autophagy inhibitor or knockdown of SHMT2 in patient-derived and CRC cell xenograft models. Our findings identified the low SHMT2-induced autophagy on 5-FU resistance in CRC. These results reveal SHMT2-p53 as a novel cancer therapeutic target to reduce chemotherapeutic drug resistance.

cancer biology↗