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Your search keyword '"Shang, Yutong"' showing total 14 results
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14 results on '"Shang, Yutong"'

10. Genome-Wide Identification and Analysis of the MAPK and MAPKK Gene Families in Potato (Solanum tuberosum L.).

Author

Shang, Yutong, Luo, Xiaobo, Zhang, Heng, Chen, Mingjun, Yin, Wang, Cao, Zhenju, Deng, Renju, Li, Yan, and Li, Fei

Subjects
*POTATOES, *GENE families, *MITOGEN-activated protein kinases, *TUBER crops, *CHROMOSOME analysis, *PLANT growth
Abstract

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]

Published
2023
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11. NMR identification of a conserved Drp1 cardiolipin-binding motif essential for stress-induced mitochondrial fission

Author

National Institutes of Health (US), Achievement Rewards for College Scientists Foundation, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Eusko Jaurlaritza, Universidad del País Vasco, Mahajan, Mukesh, Bharambe, Nikhil, Shang, Yutong, Lu, Bin, Mandal, Abhishek, Madan Mohan, Pooja, Wang, Rihua, Boatz, Jennifer C., Martínez Gálvez, Juan Manuel, Shnyrova, Anna V., Qi, Xin, Buck, Matthias, Wel, Patrick C. A. van der, Ramachandran, Rajesh, National Institutes of Health (US), Achievement Rewards for College Scientists Foundation, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), European Commission, Eusko Jaurlaritza, Universidad del País Vasco, Mahajan, Mukesh, Bharambe, Nikhil, Shang, Yutong, Lu, Bin, Mandal, Abhishek, Madan Mohan, Pooja, Wang, Rihua, Boatz, Jennifer C., Martínez Gálvez, Juan Manuel, Shnyrova, Anna V., Qi, Xin, Buck, Matthias, Wel, Patrick C. A. van der, and Ramachandran, Rajesh

Abstract

Mitochondria form tubular networks that undergo coordinated cycles of fission and fusion. Emerging evidence suggests that a direct yet unresolved interaction of the mechanoenzymatic GTPase dynamin-related protein 1 (Drp1) with mitochondrial outer membrane-localized cardiolipin (CL), externalized under stress conditions including mitophagy, catalyzes essential mitochondrial hyperfragmentation. Here, using a comprehensive set of structural, biophysical, and cell biological tools, we have uncovered a CL-binding motif (CBM) conserved between the Drp1 variable domain (VD) and the unrelated ADP/ATP carrier (AAC/ANT) that intercalates into the membrane core to effect specific CL interactions. CBM mutations that weaken VD-CL interactions manifestly impair Drp1-dependent fission under stress conditions and induce "donut" mitochondria formation. Importantly, VD membrane insertion and GTP-dependent conformational rearrangements mediate only transient CL nonbilayer topological forays and high local membrane constriction, indicating that Drp1-CL interactions alone are insufficient for fission. Our studies establish the structural and mechanistic bases of Drp1-CL interactions in stress-induced mitochondrial fission.

Published
2021

12. Construction of Yarrowia lipolyticaand microbial consortia for degradation of n-hexadecane

Author

Shang, Yutong, Wang, Yan, Zhang, Ni, Liu, Fei, Ding, Mingzhu, and Yuan, Yingjin

Abstract

Bioremediation is a promising technology to treat the petroleum hydrocarbon contamination. In this study, the strengthen of alkane metabolism and transport activity in Yarrowia lipolyticaresulted in increased degradation of n-hexadecane. The highest degradation rate of 10 g/L n-hexadecane of engineered Y. lipolyticawas 75.12 % at 96 h, and the wild-type was 45 %. Candida bombicola,which could produce sophorolipids, was cultured with the engineered Y. lipolyticato construct microbial consortia for improving the degradation. The highest degradation rate by the microbial consortia reached 81.57 % at 96 h. Transcriptomic analysis showed the expression levels of genes related to alkane metabolism in engineered Y. lipolyticawas down-regulated. Thus, the alcohol dehydrogenase activity was further strengthened, and the degradation rate of 20 g/L n-hexadecane were significantly increased. The 20 g/L n-hexadecane degradation rate of newly engineered Y. lipolyticareached 57.89 %, and that of the microbial consortium reached 72.28 %. This study provides new insights into the construction of synthetic microbial consortia for high-efficient degradation of n-hexadecane.

Published
2024
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13. Regulation of MICOS Complex in Neurodegenerative Diseases

Author

Shang, Yutong

Subjects
Biology, Biomedical Research, Molecular Biology, Neurosciences, Pathology, Physiology, Cellular Biology, Alzheimer’s disease, Huntington's disease, mitochondria, MICOS complex, neuroprotection, neurodegeneration
Abstract

Neurodegenerative diseases are nervous system disorders characterized by selective types of neuronal cell death. The causal factors for the different diseases vary, and clear molecular and cellular pathways underlying the pathogeneses remain elusive. However, accumulating evidence has suggested that mitochondrial dysfunction plays a critical role in disease-associated cell death due to the enormous energy demands of neurons. To improve the efficiency of oxidative respiration and generate more ATP, proteins on mitochondrial inner membrane form a complex adjacent to cristae junction. This complex, called the mitochondrial contact site and cristae organizing system (MICOS), maintains proper cristae morphology and stabilizes the intracristal environment for important mitochondrial functions, such as oxidative respiration. Previous studies have revealed that disruption of the MICOS leads to similar mitochondrial defects as in neurodegenerative diseases. This suggests MICOS loss as an upstream event of mitochondrial dysfunction and neuronal cell death in these disorders.In the present study, MICOS disruption was found in both Alzheimer’s disease (AD) and Huntington’s disease (HD) with different target components and molecular mechanisms. CHCHD6 was specifically connected to AD through a feedback loop that lowered CHCHD6 levels and increased APP processing. In cellular and animal AD models and human AD brains, the APP intracellular domain fragment inhibited CHCHD6 transcription by binding its promoter. CHCHD6 and APP bound to and stabilized each other. Reduced CHCHD6 enhanced APP accumulation on mitochondria-associated ER membranes and accelerated APP processing and induced mitochondrial dysfunction and neuronal cholesterol accumulation, promoting the amyloid pathology. Compensation for CHCHD6 loss in an AD mouse model ameliorated the AD-associated neuropathology and cognitive impairment. In contrast to AD, the specific MICOS component contributing to MICOS loss in HD was mitofilin. Consistent loss of mitofilin was found in HD cells, mice, and patients. Overexpression of mitofilin rescued mitochondrial dysfunction in HD cells and reduced neuropathology and motor deficits in HD mice. Even though different disease-causing factors impair different components of the MICOS, the assembly of the complex was consistently lost. Thus, our findings reveal that targeting the MICOS complex may be a potential translational strategy in neurodegenerative diseases..

Published
2023

14. Proteomimetic polymer blocks mitochondrial damage, rescues Huntington's neurons, and slows onset of neuropathology in vivo.

Author

Choi W, Fattah M, Shang Y, Thompson MP, Carrow KP, Hu D, Liu Z, Avram MJ, Bailey K, Berger O, Qi X, and Gianneschi NC

Subjects
Animals, Mice, Humans, Polymers chemistry, Polymers pharmacology, Valosin Containing Protein metabolism, Valosin Containing Protein antagonists & inhibitors, Peptides pharmacology, Peptides chemistry, Huntington Disease metabolism, Huntington Disease drug therapy, Huntington Disease pathology, Mitochondria metabolism, Mitochondria drug effects, Neurons metabolism, Neurons drug effects, Neurons pathology, Mice, Transgenic, Disease Models, Animal, Huntingtin Protein genetics, Huntingtin Protein metabolism
Abstract

Recently, it has been shown that blocking the binding of valosin-containing protein (VCP) to mutant huntingtin (mtHtt) can prevent neuronal mitochondrial autophagy in Huntington's disease (HD) models. Herein, we describe the development and efficacy of a protein-like polymer (PLP) for inhibiting this interaction in cellular and in vivo models of HD. PLPs exhibit bioactivity in HD mouse striatal cells by successfully inhibiting mitochondrial destruction. PLP is notably resilient to in vitro enzyme, serum, and liver microsome stability assays, which render analogous control oligopeptides ineffective. PLP demonstrates a 2000-fold increase in circulation half-life compared to peptides, exhibiting an elimination half-life of 152 hours. In vivo efficacy studies in HD transgenic mice (R6/2) confirm the superior bioactivity of PLP compared to free peptide through behavioral and neuropathological analyses. PLP functions by preventing pathologic VCP/mtHtt binding in HD animal models; exhibits enhanced efficacy over the parent, free peptide; and implicates the PLP as a platform with potential for translational central nervous system therapeutics.

Published
2024
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