RESUMEN
One of the most serious consequences of eutrophication in shallow lakes is deterioration of water quality, proliferation of phytoplankton and disappearance of submerged macrophytes. After removing herbivorous and plankti-benthivorous fish, submerged macrophyte restoration was utilized at the entire lake (82.7 km2) to combat eutrophication and improve water quality in the shallow subtropical aquaculture of Lake Datong. We conducted two years of monitoring, from March 2018 to February 2020. During the first year of restoration, 80% of the area of Lake Datong (approximately 60 km2) was successfully recovered by submerged vegetation, and the water quality was improved. For example, the phosphorous (P) content (including total P (TP), dissolved reactive P (DRP) and total dissolved P (TDP)) and turbidity decreased, and the Secchi depth (SD) increased. However, the submerged vegetation disappeared from autumn 2019 in the intermittent recovery area (MN), while the continuous recovery area (DX) continued to recover with an abundance of submerged vegetation. During the second year, the water quality continued to improve significantly in the DX area, with high biomass and coverage of submerged vegetation. In the MN area, although turbidity and ammonia nitrogen (NH4+-N) increased significantly and SD decreased significantly, the P content (TP, TDP, and DRP) still continued to decrease. The restoration of submerged macrophytes could significantly decrease the density of phytoplankton. Over time, there was a regime shift in Lake Datong. The structural equation model (SEM) results illustrated that the water level and submerged plant coverage were the primary drivers that triggered changes in the state of the lake ecosystem. Our results highlight the potential of restoring submerged vegetation to control water eutrophication at the whole-lake scale. However, the water level in spring was the primary driver that triggered changes in the state of the lake ecosystem. Water level management should be emphasized during the early stages of recovery of submerged plants.
Asunto(s)
Lagos , Fitoplancton , Animales , China , Ecosistema , Eutrofización , Fósforo/análisis , Calidad del AguaRESUMEN
Acetaminophen (APAP) overdose is one of the leading causes of hepatotoxicity and acute liver failure in the United States. Accumulating evidence suggests that hepatocyte necrosis plays a critical role in APAP-induced liver injury (AILI). However, the mechanisms of APAP-induced necrosis and liver injury are not fully understood. In this study, we found that p53 up-regulated modulator of apoptosis (PUMA), a B-cell lymphoma-2 (Bcl-2) homology domain 3 (BH3)-only Bcl-2 family member, was markedly induced by APAP in mouse livers and in isolated human and mouse hepatocytes. PUMA deficiency suppressed APAP-induced mitochondrial dysfunction and release of cell death factors from mitochondria, and protected against APAP-induced hepatocyte necrosis and liver injury in mice. PUMA induction by APAP was p53 independent, and required receptor-interacting protein kinase 1 (RIP1) and c-Jun N-terminal kinase (JNK) by transcriptional activation. Furthermore, a small-molecule PUMA inhibitor, administered after APAP treatment, mitigated APAP-induced hepatocyte necrosis and liver injury. Conclusion: Our results demonstrate that RIP1/JNK-dependent PUMA induction mediates AILI by promoting hepatocyte mitochondrial dysfunction and necrosis, and suggest that PUMA inhibition is useful for alleviating acute hepatotoxicity attributed to APAP overdose.
Asunto(s)
Acetaminofén/envenenamiento , Analgésicos no Narcóticos/envenenamiento , Proteínas Reguladoras de la Apoptosis/metabolismo , Enfermedad Hepática Inducida por Sustancias y Drogas/metabolismo , Proteínas Supresoras de Tumor/metabolismo , Animales , Proteínas Reguladoras de la Apoptosis/antagonistas & inhibidores , Enfermedad Hepática Inducida por Sustancias y Drogas/tratamiento farmacológico , Enfermedad Hepática Inducida por Sustancias y Drogas/etiología , Enfermedad Hepática Inducida por Sustancias y Drogas/patología , Evaluación Preclínica de Medicamentos , Proteínas Activadoras de GTPasa/metabolismo , Hígado/ultraestructura , Sistema de Señalización de MAP Quinasas , Masculino , Ratones Noqueados , Proteínas Supresoras de Tumor/antagonistas & inhibidoresRESUMEN
Compliance with ethical standards: This study did not involve human participants and animals, and the plant of interest is not an endangered species. Polygalacturonase-inhibiting proteins (PGIPs) are leucine-rich repeat proteins that plants produce against polygalacturonase, a key virulence agent in pathogens. In this paper, we cloned and purified CkPGIP1, a gene product from Cynanchum komarovii that effectively inhibits polygalacturonases from Botrytis cinerea and Rhizoctonia solani. We found the expression of CkPGIP1 to be induced in response to salicylic acid, wounding, and infection with B. cinerea and R. solani. In addition, transgenic overexpression in Arabidopsis enhanced resistance against B. cinerea. Furthermore, CkPGIP1 obtained from transgenic Arabidopsis inhibited the activity of B. cinerea and R. solani polygalacturonases by 62.7-66.4% and 56.5-60.2%, respectively. Docking studies indicated that the protein interacts strongly with the B1-sheet at the N-terminus of the B. cinerea polygalacturonase, and with the C-terminus of the polygalacturonase from R. solani. This study highlights the significance of CkPGIP1 in plant disease resistance, and its possible application to manage fungal pathogens.
Asunto(s)
Arabidopsis/microbiología , Cynanchum/metabolismo , Enfermedades de las Plantas/microbiología , Extractos Vegetales/química , Proteínas de Plantas/metabolismo , Secuencia de Aminoácidos , Botrytis/enzimología , Clonación Molecular , Cynanchum/genética , Resistencia a la Enfermedad/genética , Regulación de la Expresión Génica , Concentración 50 Inhibidora , Simulación del Acoplamiento Molecular , Datos de Secuencia Molecular , Filogenia , Proteínas de Plantas/genética , Plantas Modificadas Genéticamente , Poligalacturonasa/antagonistas & inhibidores , Reacción en Cadena de la Polimerasa , Unión Proteica , Estructura Terciaria de Proteína , Rhizoctonia/enzimología , Ácido Salicílico/química , Homología de Secuencia de AminoácidoRESUMEN
Cynanchum komarovii Al Iljinski is a desert plant that has been used as analgesic, anthelminthic, and antidiarrheal, but also as herbal medicine to treat cholecystitis in people. In this work, an antifungal protein with sequence homology to chitinase was isolated from C. komarovii seeds and named CkChn134. The three-dimensional structure prediction of CkChn134 indicated that the protein has a loop domain formed a thin cleft, which is able to bind molecules and substrates. The protein and CkTLP synergistically inhibited the fungal growth of Verticillium dahliae, Fusarium oxysporum, Rhizoctonia solani, Botrytis cinerea, and Valsa mali in vitro. The full-length cDNA was cloned by RT-PCR and RACE-PCR according to the partial protein sequences obtained by nanoESI-MS/MS. The real-time PCR showed that the transcription level of CkChn134 had a significant increase under the stress of ethylene, NaCl, low temperature, drought, and pathogen infection, which indicates that CkChn134 may play an important role in response to abiotic and biotic stresses. The CkChn134 protein was located in the extracellular space/cell wall by CkChn134::GFP fusion protein in transgenic Arabidopsis. Furthermore, overexpression of CkChn134 significantly enhanced the resistance of transgenic Arabidopsis against V. dahliae. Interestingly, the coexpression of CkChn134 and CkTLP showed substantially greater protection against the fungal pathogen V. dahliae than either transgene alone. The results suggest that the CkChn134 is a good candidate protein or gene, and it had a potential synergistic effect with CkTLP for contributing to the development of disease-resistant crops.