{"title":"氨基甲酰化促进α-Synuclein KTKEGV重复基序的序列特异性淀粉样蛋白形成。","authors":"Joshna Gadhavi, , , Sumedha Shah, , , Mohini Patel, , and , Sharad Gupta*, ","doi":"10.1021/acschemneuro.5c00561","DOIUrl":null,"url":null,"abstract":"<p >KTKEGV repeat motifs play a crucial role in regulating the folding of α-synuclein structure and function, including tetramer formation and interaction with membranes. In α-syn, nine KTKEGV imperfect repeats have been reported. Post-translational modifications (PTMs) that could neutralize the positive charge on lysine may disturb the electrostatic interaction of α-syn with the cellular membrane, thereby affecting physiological function. Carbamylation is one such nonenzymatic age-dependent charge-neutralizing PTM which is reported to be elevated in aged people. While some reports have suggested that carbamylation is a proaggregation factor, others have assigned it a protective role. In the present study, we explored the aggregation propensities of KTKEGV repeat motifs and full-length α-syn protein upon carbamylation. We observed distinct aggregation kinetics among various KTKEGV motifs of α-syn, including disease-specific mutated versions, which was confirmed by multiple biophysical techniques such as ThT assay, turbidity measurement, Congo red staining, AFM, and SEM. Notably, the repeat motifs 3 (<sup>32</sup>KTKEGVLYV<sup>40</sup>), 5 (<sup>58</sup>KTKEQVTNV<sup>66</sup>), and the core motif (<sup>77</sup>VAQKTV<sup>82</sup>) exhibited robust fibrillar amyloid formation when carbamylated. Also, repeat motif 4 (<sup>43</sup>KTKEGVVH<sup>50</sup>), when mutated (E46K, H50Q, and both), becomes an aggregation hotspot, even though the native sequence does not aggregate upon carbamylation. Carbamylation of full-length α-syn protein appears to lead to aggregation with higher fibrillar amyloid content as indicated by a several-fold enhancement of ThT plateau fluorescence. Such carbamylated α-syn aggregates could recruit unmodified α-syn and again led to the formation of well-organized amyloid fibrils. These findings highlight the site-specific role of charge-neutralizing PTMs such as carbamylation α-syn aggregation and provide novel insights into the molecular mechanisms related to synucleinopathies and dementia with Lewy bodies.</p>","PeriodicalId":13,"journal":{"name":"ACS Chemical Neuroscience","volume":"16 19","pages":"3861–3872"},"PeriodicalIF":3.9000,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Carbamylation Promotes Sequence-Specific Amyloidogenesis in the α-Synuclein KTKEGV Repeat Motifs\",\"authors\":\"Joshna Gadhavi, , , Sumedha Shah, , , Mohini Patel, , and , Sharad Gupta*, \",\"doi\":\"10.1021/acschemneuro.5c00561\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p >KTKEGV repeat motifs play a crucial role in regulating the folding of α-synuclein structure and function, including tetramer formation and interaction with membranes. In α-syn, nine KTKEGV imperfect repeats have been reported. Post-translational modifications (PTMs) that could neutralize the positive charge on lysine may disturb the electrostatic interaction of α-syn with the cellular membrane, thereby affecting physiological function. Carbamylation is one such nonenzymatic age-dependent charge-neutralizing PTM which is reported to be elevated in aged people. While some reports have suggested that carbamylation is a proaggregation factor, others have assigned it a protective role. In the present study, we explored the aggregation propensities of KTKEGV repeat motifs and full-length α-syn protein upon carbamylation. We observed distinct aggregation kinetics among various KTKEGV motifs of α-syn, including disease-specific mutated versions, which was confirmed by multiple biophysical techniques such as ThT assay, turbidity measurement, Congo red staining, AFM, and SEM. Notably, the repeat motifs 3 (<sup>32</sup>KTKEGVLYV<sup>40</sup>), 5 (<sup>58</sup>KTKEQVTNV<sup>66</sup>), and the core motif (<sup>77</sup>VAQKTV<sup>82</sup>) exhibited robust fibrillar amyloid formation when carbamylated. Also, repeat motif 4 (<sup>43</sup>KTKEGVVH<sup>50</sup>), when mutated (E46K, H50Q, and both), becomes an aggregation hotspot, even though the native sequence does not aggregate upon carbamylation. Carbamylation of full-length α-syn protein appears to lead to aggregation with higher fibrillar amyloid content as indicated by a several-fold enhancement of ThT plateau fluorescence. Such carbamylated α-syn aggregates could recruit unmodified α-syn and again led to the formation of well-organized amyloid fibrils. These findings highlight the site-specific role of charge-neutralizing PTMs such as carbamylation α-syn aggregation and provide novel insights into the molecular mechanisms related to synucleinopathies and dementia with Lewy bodies.</p>\",\"PeriodicalId\":13,\"journal\":{\"name\":\"ACS Chemical Neuroscience\",\"volume\":\"16 19\",\"pages\":\"3861–3872\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2025-09-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Chemical Neuroscience\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://pubs.acs.org/doi/10.1021/acschemneuro.5c00561\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Chemical Neuroscience","FirstCategoryId":"3","ListUrlMain":"https://pubs.acs.org/doi/10.1021/acschemneuro.5c00561","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Carbamylation Promotes Sequence-Specific Amyloidogenesis in the α-Synuclein KTKEGV Repeat Motifs
KTKEGV repeat motifs play a crucial role in regulating the folding of α-synuclein structure and function, including tetramer formation and interaction with membranes. In α-syn, nine KTKEGV imperfect repeats have been reported. Post-translational modifications (PTMs) that could neutralize the positive charge on lysine may disturb the electrostatic interaction of α-syn with the cellular membrane, thereby affecting physiological function. Carbamylation is one such nonenzymatic age-dependent charge-neutralizing PTM which is reported to be elevated in aged people. While some reports have suggested that carbamylation is a proaggregation factor, others have assigned it a protective role. In the present study, we explored the aggregation propensities of KTKEGV repeat motifs and full-length α-syn protein upon carbamylation. We observed distinct aggregation kinetics among various KTKEGV motifs of α-syn, including disease-specific mutated versions, which was confirmed by multiple biophysical techniques such as ThT assay, turbidity measurement, Congo red staining, AFM, and SEM. Notably, the repeat motifs 3 (32KTKEGVLYV40), 5 (58KTKEQVTNV66), and the core motif (77VAQKTV82) exhibited robust fibrillar amyloid formation when carbamylated. Also, repeat motif 4 (43KTKEGVVH50), when mutated (E46K, H50Q, and both), becomes an aggregation hotspot, even though the native sequence does not aggregate upon carbamylation. Carbamylation of full-length α-syn protein appears to lead to aggregation with higher fibrillar amyloid content as indicated by a several-fold enhancement of ThT plateau fluorescence. Such carbamylated α-syn aggregates could recruit unmodified α-syn and again led to the formation of well-organized amyloid fibrils. These findings highlight the site-specific role of charge-neutralizing PTMs such as carbamylation α-syn aggregation and provide novel insights into the molecular mechanisms related to synucleinopathies and dementia with Lewy bodies.
期刊介绍:
ACS Chemical Neuroscience publishes high-quality research articles and reviews that showcase chemical, quantitative biological, biophysical and bioengineering approaches to the understanding of the nervous system and to the development of new treatments for neurological disorders. Research in the journal focuses on aspects of chemical neurobiology and bio-neurochemistry such as the following:
Neurotransmitters and receptors
Neuropharmaceuticals and therapeutics
Neural development—Plasticity, and degeneration
Chemical, physical, and computational methods in neuroscience
Neuronal diseases—basis, detection, and treatment
Mechanism of aging, learning, memory and behavior
Pain and sensory processing
Neurotoxins
Neuroscience-inspired bioengineering
Development of methods in chemical neurobiology
Neuroimaging agents and technologies
Animal models for central nervous system diseases
Behavioral research