An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases

TDP-43 is linked to human diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD). Expression of TDP-43 in yeast is known to be toxic, cause cells to elongate, form liquid-like aggregates, and inhibit autophagy and TOROID formation. Here, we used the apt1∆ aah1∆ ye...

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Main Authors: Sangeun Park, Sei-Kyoung Park, Peter Blair, Susan W. Liebman
Format: Article
Language:English
Published: Shared Science Publishers OG 2025-05-01
Series:Microbial Cell
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Online Access:http://microbialcell.com/researcharticles/2025a-park-microbial-cell
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author Sangeun Park
Sei-Kyoung Park
Peter Blair
Susan W. Liebman
author_facet Sangeun Park
Sei-Kyoung Park
Peter Blair
Susan W. Liebman
author_sort Sangeun Park
collection DOAJ
description TDP-43 is linked to human diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD). Expression of TDP-43 in yeast is known to be toxic, cause cells to elongate, form liquid-like aggregates, and inhibit autophagy and TOROID formation. Here, we used the apt1∆ aah1∆ yeast model of inborn errors of metabolism, previously shown to lead to intracellular adenine accumulation and adenine amyloid-like fiber formation, to explore interactions with TDP-43. Results show that the double deletion shifts the TDP-43 aggregates from liquid-like droplets toward a more amyloid-like state. At the same time the deletions reduce TDP-43’s effects on toxicity, cell morphology, autophagy, and TOROID formation without affecting the level of TDP-43. This suggests that the liquid-like droplets rather than amyloid-like TDP-43 aggregates are responsible for the deleterious effects in yeast. How the apt1∆ aah1∆ deletions alter TDP-43 aggregate formation is not clear. Possibly, it results from adenine and TDP-43 fiber interactions as seen for other heterologous fibers. This work offers new insights into the potential interactions between metabolite-based amyloids and pathological protein aggregates, with broad implications for understanding protein misfolding diseases.
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institution Kabale University
issn 2311-2638
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publishDate 2025-05-01
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series Microbial Cell
spelling doaj-art-e1df3483412b47e9b9c45b2de9f8093d2025-08-20T03:53:47ZengShared Science Publishers OGMicrobial Cell2311-26382025-05-011211913110.15698/mic2025.05.850An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseasesSangeun Park0Sei-Kyoung Park1Peter Blair2Susan W. Liebman3Department of Pharmacology, University of Nevada, Reno, United States of America.Department of Pharmacology, University of Nevada, Reno, United States of America.Department of Pharmacology, University of Nevada, Reno, United States of America.Department of Pharmacology, University of Nevada, Reno, United States of America.TDP-43 is linked to human diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal degeneration (FTD). Expression of TDP-43 in yeast is known to be toxic, cause cells to elongate, form liquid-like aggregates, and inhibit autophagy and TOROID formation. Here, we used the apt1∆ aah1∆ yeast model of inborn errors of metabolism, previously shown to lead to intracellular adenine accumulation and adenine amyloid-like fiber formation, to explore interactions with TDP-43. Results show that the double deletion shifts the TDP-43 aggregates from liquid-like droplets toward a more amyloid-like state. At the same time the deletions reduce TDP-43’s effects on toxicity, cell morphology, autophagy, and TOROID formation without affecting the level of TDP-43. This suggests that the liquid-like droplets rather than amyloid-like TDP-43 aggregates are responsible for the deleterious effects in yeast. How the apt1∆ aah1∆ deletions alter TDP-43 aggregate formation is not clear. Possibly, it results from adenine and TDP-43 fiber interactions as seen for other heterologous fibers. This work offers new insights into the potential interactions between metabolite-based amyloids and pathological protein aggregates, with broad implications for understanding protein misfolding diseases.http://microbialcell.com/researcharticles/2025a-park-microbial-cellyeasttdp-43liquid-like dropletsmetabolite-based amyloidsfrapmetabolism disordersals
spellingShingle Sangeun Park
Sei-Kyoung Park
Peter Blair
Susan W. Liebman
An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
Microbial Cell
yeast
tdp-43
liquid-like droplets
metabolite-based amyloids
frap
metabolism disorders
als
title An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
title_full An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
title_fullStr An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
title_full_unstemmed An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
title_short An adenine model of inborn metabolism errors alters TDP-43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
title_sort adenine model of inborn metabolism errors alters tdp 43 aggregation and reduces its toxicity in yeast revealing insights into protein misfolding diseases
topic yeast
tdp-43
liquid-like droplets
metabolite-based amyloids
frap
metabolism disorders
als
url http://microbialcell.com/researcharticles/2025a-park-microbial-cell
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