Ultrastructural Alterations in Arabidopsis thaliana dj1c Null Mutant Cotyledons

Authors

Han Chen, University of Nebraska-LincolnFollow
J. L. Frey, University of Nebraska-Lincoln
Tara Nazarenus, University of Nebraska-LincolnFollow
Christian Elowsky, University of Nebraska-LincolnFollow
Julie M. Stone, University of Nebraska-LincolnFollow

ORCID IDs

Christian Elowsky

Date of this Version

2008

Comments

Published by Microsc Microanal 14(Suppl 2), 2008. Copyright 2008 Microscopy Society of America. Used by permission.

Abstract

Increasing evidence suggests that deficits in mitochondrial function, oxidative and nitrosative stress, accumulation of aberrant or misfolded proteins, and ubiquitin-proteasome system dysfunction may represent the principal molecular pathways that commonly underlie the pathogenesis of neurodegenerative Parkinson’s disease (PD). Mutations in human DJ-1 lead to early onset PD. The subcellular distribution of DJ-1 (PARK7) is primarily cytoplasmic with smaller quantities found associated with mitochondria. Postulated functions include roles in the oxidative stress response, either as a redox sensor protein that can prevent the aggregation of alpha-synuclein or as an antioxidant. Homologs of DJ-1 are found in all kingdoms of life. To understand the functions of plant DJ-1 homologs we identified null mutants in the model plant Arabidopsis thaliana. One of the 3 Arabidopsis genes encoding DJ1 homologs (DJ1C) is essential for viability, and null knockout mutants are seedling lethal.