RESUMEN
Ring rot, caused by Botryosphaeria dothidea, is an important fungal disease of pear fruit during postharvest storage. Melatonin, as a plant growth regulator, plays an important role in enhancing the stress resistance of pear fruits. It enhances the resistance of pear fruits to ring rot by enhancing their antioxidant capacity. However, the underlying mechanism remains unclear. In this study, we examined the effect of melatonin on the growth of B. dothidea. Results showed that melatonin did not limit the growth of B. dothidea during in vitro culture. However, metabolomics and transcriptomics analyses of 'Whangkeumbae' pear (Pyrus pyrifolia) revealed that melatonin increased the activity of antioxidant enzymes, including peroxidase (POD), superoxide dismutase (SOD), and polyphenol oxidase (PPO), in the fruit and activated the phenylpropanoid metabolic pathway to improve fruit resistance. Furthermore, melatonin treatment significantly increased the contents of jasmonic acid and phlorizin in pear fruit, both of which could improve disease resistance. Jasmonic acid regulates melatonin synthesis and can also promote phlorizin synthesis, ultimately improving the resistance of pear fruit to ring rot. In summary, the interaction between melatonin and jasmonic acid and phlorizin enhances the antioxidant defense response and phenylpropanoid metabolism pathway of pear fruit, thereby enhancing the resistance of pear fruit to ring rot disease. Our results provide new insights into the application of melatonin in the resistance to pear fruit ring rot.
Asunto(s)
Ascomicetos , Ciclopentanos , Resistencia a la Enfermedad , Frutas , Melatonina , Oxilipinas , Florizina , Enfermedades de las Plantas , Pyrus , Pyrus/microbiología , Pyrus/metabolismo , Pyrus/genética , Ciclopentanos/metabolismo , Ciclopentanos/farmacología , Oxilipinas/metabolismo , Ascomicetos/fisiología , Melatonina/farmacología , Melatonina/metabolismo , Resistencia a la Enfermedad/efectos de los fármacos , Enfermedades de las Plantas/microbiología , Frutas/microbiología , Frutas/metabolismo , Florizina/farmacología , Regulación de la Expresión Génica de las Plantas/efectos de los fármacos , Antioxidantes/metabolismo , Reguladores del Crecimiento de las Plantas/metabolismoRESUMEN
BACKGROUND: Colorectal cancer is one of the most common gastrointestinal malignancies worldwide. LRCH4 is the top 1 gene associated with an unfavorable prognosis in colorectal cancer. METHODS: Here, we reported that the knockdown of LRCH4 inhibited the proliferation, migration and invasion in HT29 cells. RESULTS: The activity of Yes-Associated Protein (YAP), a transcription factor in the Hppo-YAP signaling pathway, was significantly inhibited by LRCH4-siRNA. LRCH4 knockdown also reversed the EMT and regulated the expression of extracellular matrix (ECM) protein, Fibronectin and Collagen IV in HT29 cells. In addition, the TGF-ß/Smad signaling pathway, as the downstream pathway of Yap, was also inhibited by LRCH4 knockdown. CONCLUSION: Knockdown of LRCH4 involved in the regulation of ECM and EMT and inhibited YAP and the TGF-ß/Smad signaling pathway in colorectal cancer cells. Our study provided a mechanism of LRCH4 on colorectal cancer cells, and a new potential target for clinical tumor treatment.
Asunto(s)
Proliferación Celular , Neoplasias Colorrectales , Transducción de Señal , Proteínas Smad , Factores de Transcripción , Factor de Crecimiento Transformador beta , Microambiente Tumoral , Humanos , Neoplasias Colorrectales/patología , Neoplasias Colorrectales/metabolismo , Neoplasias Colorrectales/genética , Factor de Crecimiento Transformador beta/metabolismo , Factores de Transcripción/metabolismo , Factores de Transcripción/genética , Proteínas Smad/metabolismo , Proteínas Señalizadoras YAP , Movimiento Celular , Proteínas Adaptadoras Transductoras de Señales/metabolismo , Proteínas Adaptadoras Transductoras de Señales/genética , Técnicas de Silenciamiento del Gen , Células HT29RESUMEN
Defects formed at the surface, buried interface and grain boundaries (GB) of CsPbI3 perovskite films considerably limit photovoltaic performance. Such defects could be passivated effectively by the most prevalent post modification strategy without compromising the photoelectric properties of perovskite films, but it is still a great challenge to make this strategy comprehensive to different defects spatially distributed throughout the films. Herein, a spatially selective defect management (SSDM) strategy is developed to roundly passivate various defects at different locations within the perovskite film by a facile one-step treatment procedure using a piperazine-1,4-diium tetrafluoroborate (PZD(BF4)2) solution. The small-size PZD2+ cations could penetrate into the film interior and even make it all the way to the buried interface of CsPbI3 perovskite films, while the BF4- anions, with largely different properties from I- anions, mainly anchor on the film surface. Consequently, virtually all the defects at the surface, buried interface and grain boundaries of CsPbI3 perovskite films are effectively healed, leading to significantly improved film quality, enhanced phase stability, optimized energy level alignment and promoted carrier transport. With these films, the fabricated CsPbI3 PSCs based on carbon electrode (C-PSCs) achieve an efficiency of 18.27%, which is among the highest-reported values for inorganic C-PSCs, and stability of 500 h at 85 °C with 65% efficiency maintenance.