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Mitogen-activated protein kinase (MAPK) is an important component of the signal transduction pathway, which plays important roles in regulating plant growth and development, and abiotic stress. Potato (Solanum tuberosum L.) is one of the most popular tuber crops in the world. Genome-wide identification and analysis of the MAPK and MAPKK gene family in potato is not clear. A total of 20 MAPK genes and 8 MAPKK genes were identified in the potato genome. A conservative motif analysis showed that the MAPK protein contained a typical TxY phosphorylation site, and the MAPKK protein contained a conservative characteristic motif S/T-x5-S/T. Phylogenetic analysis showed that potato MAPK (mitogen-activated protein kinase) and MAPKK (mitogen-activated protein kinase kinase) were similar to Arabidopsis, including four groups of members A, B, C and D. Gene structure and promoter sequence analysis showed that all 28 gene family members of potato Solanum tuberosum MAPK (StMAPK) and StMAPKK have coding regions (CDS), and family members in the same group have similar intron and exon compositions, and that most cis-acting elements upstream of gene promoters elements have related to stress response. Chromosome location analysis found that MAPKs were unevenly distributed on 11 chromosomes, while MAPKKs were only distributed on chromosomes Chr. 03 and Chr. 12. Collinearity analysis showed that StMAPKK3 and StMAPKK6 have the same common ancestors among potato, pepper, and tomato. qRT-PCR results showed that the relative expressions of StMAPK14 and StMAPKK2 were significantly upregulated under low-temperature stress. These results could provide new insights into the characteristics and evolution of the StMAPK and StMAPKK gene family and facilitate further exploration of the molecular mechanism responsible for potato abiotic stress responses. [ABSTRACT FROM AUTHOR]

The mechanistic relationship between amyloid-beta precursor protein (APP) processing and mitochondrial dysfunction in Alzheimer's disease (AD) has long eluded the field. Here, we report that coiled-coil-helix-coiled-coil-helix domain containing 6 (CHCHD6), a core protein of the mammalian mitochondrial contact site and cristae organizing system, mechanistically connects these AD features through a circular feedback loop that lowers CHCHD6 and raises APP processing. In cellular and animal AD models and human AD brains, the APP intracellular domain fragment inhibits CHCHD6 transcription by binding its promoter. CHCHD6 and APP bind and stabilize one another. Reduced CHCHD6 enhances APP accumulation on mitochondria-associated ER membranes and accelerates APP processing, and induces mitochondrial dysfunction and neuronal cholesterol accumulation, promoting amyloid pathology. Compensation for CHCHD6 loss in an AD mouse model reduces AD-associated neuropathology and cognitive impairment. Thus, CHCHD6 connects APP processing and mitochondrial dysfunction in AD. This provides a potential new therapeutic target for patients. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function. Our findings reveal a consistent downregulation of BCKDK in dopaminergic (DA) neurons from A53T-αSyn mouse models, PD patient-derived induced pluripotent stem (iPS) cells, and postmortem brain tissues. BCKDK deficiency leads to mitochondrial dysfunction, including reduced membrane potential and increased reactive oxygen species (ROS) production upon administration of a stressor, which in turn promotes αSyn oligomerization. Mechanistically, BCKDK interacts with the NDUFS1 subunit of Complex I to stabilize its function. Loss of BCKDK disrupts this interaction, leading to Complex I destabilization and enhanced αSyn aggregation. Notably, restoring BCKDK expression in neuron-like cells rescues mitochondrial integrity and restores Complex I activity. Similarly, in patient-derived iPS cells differentiated to form dopaminergic neurons, NDUFS1 and phosphorylated aSyn levels are partially restored upon BCKDK expression. These findings establish a mechanistic link between BCKDK deficiency, mitochondrial dysfunction, and αSyn pathology in PD, positioning BCKDK as a potential therapeutic target to mitigate mitochondrial impairment and neurodegeneration in PD. [ABSTRACT FROM AUTHOR]

[Display omitted] • 2D In 2 O 3 is decorated on 2D BiOBr to form a Z-scheme heterojunction. • This work achieves improved internal electric field and charge separation. • The B 3 I 1 composite exhibits enhanced photocatalytic activity. • The mechanism of photocatalytic CO 2 reduction into CO is proposed. CO 2 photocatalytic reduction is an excellent strategy for promoting solar-to-chemical energy conversion and alleviating the severe environmental crisis. In this study, 2D indium oxide (IO) is decorated on 2D bismuth oxybromide (BOB) nanosheets to gain BOB/IO (B x I y) heterojunction. The optimal B 3 I 1 composite affords a CO production rate of 54.2 μmol⋅g−1, about 2.2 times and 11.3 times higher than those of the pristine BOB and IO, respectively. The introduction of IO significantly enhances the internal electric field (IEF), leading to accelerated charge transfer and prolonged lifetime of the photogenerated carriers. In the B x I y composite, the BOB and IO serve as the electron acceptor and donor, respectively, facilitating the reduction of CO 2 and oxidation of H 2 O. In-situ DRIFTs spectra are used to confirm the catalytic active sites and provide insights into the mechanism of CO 2 photoreduction. The results suggest *COOH and *CO 2 – species played a crucial role in the formation of CO. This work presents a valuable perspective on understanding the charge transfer route and developing highly efficient photocatalysts for CO 2 photoreduction. [ABSTRACT FROM AUTHOR]

Current application of human induced pluripotent stem cells (hiPSCs) technology in patient-specific models of neurodegenerative disorders recapitulate some of key phenotypes of diseases, representing disease-specific cellular modeling and providing a unique platform for therapeutics development. We review recent efforts toward advancing hiPSCs-derived neuronal cell types and highlight their potential use for the development of more complex in vitro models of neurodegenerative diseases by focusing on Alzheimer's disease, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. We present evidence from previous works on the important phenotypic changes of various neuronal types in these neurological diseases. We also summarize efforts on conducting low- and high-throughput screening experiments with hiPSCs toward developing potential therapeutics for treatment of neurodegenerative diseases. Lastly, we discuss the limitations of hiPSCs culture system in studying neurodegenerative diseases and alternative strategies to overcome these hurdles. • The important phenotypic changes of neuronal types derived from hiPSCs of neurodegenerative diseases • Summarize the efforts on drug discovery using patient hiPSCs toward developing potential therapeutics • Discuss the limitations of hiPSCs culture system in studying neurodegenerative diseases [ABSTRACT FROM AUTHOR]

[Display omitted] • Sulfadiazine's inhibitory effect was stronger on denitrification. • Sulfadiazine's inhibitory effect was stronger on ammonia-oxidizing bacteria. • SDZ led to a decrease in the abundance of comammox bacteria (Nitrospira). • Enterobacter , Sphingomonas and Gemmatimonas are mutualistic in denitrification. • Sulfadiazine resulted in the accumulation of nitrite. Antibiotics in wastewater can affect the structures and functions of bacterial communities, subsequently influencing how well a biological process performs. Therefore, the characteristics of bacterial community were investigated in a hybrid moving bed biofilm reactor-membrane bioreactor system when treating domestic wastewater containing sulfadiazine (SDZ). Results indicated total nitrogen removal reduced by 10.2%, 9.1%, 2.7% and 2.9%, respectively, with increasing carbon to nitrogen (C/N) ratios (2.5, 4, 6 and 9) when SDZ was present (0.5 mg/L). The microbial communities' analysis revealed that the abundance of nitrogen removal-related bacteria increased with C/N. Specifically, the abundance of ammonia-oxidizing bacteria (0.46%-0.90%) was low, and the nitrite-oxidizing bacteria (2.16%-7.13%) and denitrifying bacteria showed a significant increase (Hyphomicrobium : 0.57%-3.54%) when C/N ratio increased. The abundance of denitrifying bacterial declined by 4.82–8.56% at different C/N ratios, while nitrifying bacterial rose by 0.70–5.67%. Interestingly, the denitrifying bacteria Enterobacter , Sphingomonas and Gemmatimonas acted as mutualistic bacteria that stabilized denitrification. [ABSTRACT FROM AUTHOR]

Angelica dahurica is an important Chinese herbal medicine plant, and its rhizome is of high medicinal value. In recent years, a severe decline in yield has been observed in Bozhou City ( China's largest A. dahurica producing area), Anhui province, China. It showed symptoms of decline, stunting, yellowing and many galls in the roots, which was the characterization of infestation by root-knot nematodes. A survey of root-knot nematodes on its roots was conducted in this area from June to September, 2011. Based on our results, the nematode species on A. dahurica was identified as Meloidogyne arenaria by the morphological, biochemical and molecular methods. To our knowledge, this is the first report of M. arenaria on A. dahurica in China. [ABSTRACT FROM AUTHOR]