Home LiteratureArticle Details
PMID: 16566606 Published · ppublish English Journal Article Research Support, N.I.H., Extramural

Peroxynitrite-mediated tau modifications stabilize preformed filaments and destabilize microtubules through distinct mechanisms.

Biochemistry ·Vol. 45 ·No. 13 ·2006-04-04 ·Pages 4314-26

Reynolds MR, Lukas TJ, Berry RW, Binder LI

Abstract

Alzheimer's disease (AD) is a progressive amnestic dementia typified by abnormal modifications of the microtubule (MT)-associated tau protein that promote its pathological self-assembly and displacement from the MT lattice. Previously, we showed that peroxynitrite (ONOO-) induces the oxidative 3,3'-dityrosine (3,3'-DT) cross-linking and site-selective nitration of tau monomers [Reynolds et al. (2005) Biochemistry 44, 1690-1700]. In the present study, we examined the effects of ONOO(-)-mediated modifications on two key elements of tau pathobiology: (1) the stability of preformed tau filaments and (2) the ability of monomeric tau to promote tubulin assembly. Here, we report that treatment of synthetic tau filaments with ONOO- generates heat-stable, SDS-insoluble aggregates with a significantly reduced mobility by SDS-PAGE compared to that of nontreated filaments. Ultrastructurally, these aggregates appear to be cross-linked via interfilament bridges. Using LC-MS/MS and HPLC with fluorescent detection, we demonstrate that covalent 3,3'-DT linkages are present within these higher-order aggregates. Similar to monomeric tau, filamentous tau exhibits a hierarchical pattern of nitration following ONOO- treatment with site selectivity toward the amino-terminal residues Tyr18 and Tyr29. Further, select nitration of residues Tyr18, Tyr29, Tyr197, and Tyr394, events known to stabilize the pathological Alz-50 conformation [Reynolds et al. (2005) Biochemistry 44, 13997-14009], inhibits the ability of monomeric tau to promote tubulin assembly. This effect is specific for the 3-NT modification, as mutant tau proteins pseudophosphorylated at each Tyr residue are fully competent to stabilize MTs. Collectively, our results suggest that ONOO(-)-mediated modifications stabilize tau filaments via 3,3'-DT bonding and destabilize MTs by site-selective nitration of tau monomers. Moreover, assumption of the Alz-50 conformation may be the mechanism through which tau nitration modulates MT stability.

MeSH Terms
Amino Acid Sequence Microtubules/drug effects,metabolism Neurofibrillary Tangles/drug effects Peroxynitrous Acid/pharmacology Protein Structure, Quaternary/drug effects Tyrosine/chemistry tau Proteins/chemistry,genetics,metabolism
Chemicals
tau Proteins Peroxynitrous Acid Tyrosine
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Reynolds Matthew R
Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. m-reynolds@md.northwestern.edu
Lukas Thomas J
Berry Robert W
Binder Lester I
Article Info
Journal
Biochemistry
Abbr.
Biochemistry
ISSN
0006-2960
Published
2006-04-04
Pages
4314-26
Language
English
Region
United States
NLM ID
0370623
Subset
IM
Grants
NIA NIH HHS · AG 14453 · United States
NIA NIH HHS · AG 21184 · United States
NINDS NIH HHS · F30 NS051043 · United States
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: product@genelibs.com