000282946 001__ 282946
000282946 005__ 20251218103447.0
000282946 0247_ $$2doi$$a10.5281/ZENODO.17113344
000282946 0247_ $$2doi$$a10.5281/zenodo.17113344
000282946 037__ $$aDZNE-2025-01407
000282946 1001_ $$00000-0003-1408-2214$$aRayan, Bader$$b0
000282946 245__ $$aDataset: RNA Selectively Modulates Activity of Virulent Amyloid PSMα3 and Host Defense LL-37 via Phase Separation and Aggregation Dynamics, v1
000282946 260__ $$bZenodo$$c2025
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000282946 520__ $$aAmyloids, classically linked to neurodegenerative diseases, also play critical roles in infection and immunity. Phenol-soluble modulins (PSMs) from Staphylococcus aureus are virulent amyloids that contribute to cytotoxicity, immune modulation, and biofilm stability. PSMα3 forms cross-α amyloid fibrils and shares sequence and structural features with LL-37, a human host-defense peptide that assembles into α-helical structures. Here, we uncover RNA as a potent, context-dependent modulator of their aggregation and activity. RNA consistently reduces LL-37’s cytotoxicity toward human cells without compromising its antibacterial function, suggesting a selective host-protective mechanism. In contrast, RNA preserves PSMα3’s cytotoxic and antimicrobial activity over time, likely by promoting liquid–liquid phase separation (LLPS) and stabilizing bioactive fibrillar polymorphs, enabling S. aureus to fine-tune its virulence strategies. At higher concentrations, RNA drives both peptides toward distinct aggregated states, amorphous for LL-37 and fibrillar for PSMα3, underlying their divergent functional outcomes. The amyloid inhibitor EGCG abolishes the bioactivity of both PSMα3 and LL-37, overriding RNA’s modulatory effects. Together, our findings establish RNA as a key modulator of both virulent amyloids and host-defense peptides, with broad implications for microbial immune evasion, innate immunity, and amyloid-associated diseases. Moreover, they highlight phase transitions as a tunable mechanism for regulating peptide bioactivity and a promising therapeutic target across infectious and neurodegenerative conditions.
000282946 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
000282946 588__ $$aDataset connected to DataCite
000282946 7001_ $$aBarnea, Eilon$$b1
000282946 7001_ $$aIndig, Rinat$$b2
000282946 7001_ $$0P:(DE-2719)2812808$$aPantoja, Christian Felipe$$b3
000282946 7001_ $$aGayk, Jesse$$b4
000282946 7001_ $$00000-0002-2601-4123$$aLupu-Haber, Yael$$b5
000282946 7001_ $$00000-0002-0910-6552$$aUpcher, Alexander$$b6
000282946 7001_ $$00000-0002-0412-003X$$aArgoetti, Amir$$b7
000282946 7001_ $$00000-0002-6782-0594$$aLarsen, Jacob$$b8
000282946 7001_ $$00000-0003-1161-3622$$aBuell, Alexander$$b9
000282946 7001_ $$0P:(DE-2719)2810591$$aZweckstetter, Markus$$b10
000282946 7001_ $$00000-0002-1743-3430$$aLandau, Meytal$$b11
000282946 773__ $$a10.5281/zenodo.17113344
000282946 7870_ $$0DZNE-2025-01406$$aRayan, Bader et.al.$$dZenodo, 2025$$iRelatedTo$$r$$tDataset: RNA Selectively Modulates Activity of Virulent Amyloid PSMα3 and Host Defense LL-37 via Phase Separation and Aggregation Dynamics, v2
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000282946 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2812808$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
000282946 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810591$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b10$$kDZNE
000282946 9131_ $$0G:(DE-HGF)POF4-352$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vDisease Mechanisms$$x0
000282946 9141_ $$y2025
000282946 9201_ $$0I:(DE-2719)1410001$$kAG Zweckstetter$$lTranslational Structural Biology$$x0
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