tailieunhanh - báo cáo khoa học: " Overexpression of mtDNA-associated AtWhy2 compromises mitochondrial function"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Overexpression of mtDNA-associated AtWhy2 compromises mitochondrial function | BMC Plant Biology BioMed Central Open Access Research article Overexpression of mtDNA-associated AtWhy2 compromises mitochondrial function Alexandre Maréchal Jean-Sébastien Parent Mohammed Sabar Félix Véronneau-Lafortune Charbel Abou-Rached and Normand Brisson Address Department of Biochemistry Université de Montréal 2900 Édouard-Montpetit Montréal Québec H3C 3J7 Canada Email Alexandre Maréchal - Jean-Sébastien Parent - Mohammed Sabar - Félix Véronneau-Lafortune - Charbel Abou-Rached - Normand Brisson - Corresponding author Published 18 April 2008 Received 21 September 2007 BMC Plant Biology 2008 8 42 doi 1471-2229-8-42 Accepted 18 April 2008 This article is available from http 1471-2229 8 42 2008 Maréchal et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background StWhy1 a member of the plant-specific Whirly single-stranded DNA-binding protein family was first characterized as a transcription factor involved in the activation of the nuclear PR-10a gene following defense-related stress in potato. In Arabidopsis thaliana Whirlies have recently been shown to be primarily localized in organelles. Two representatives of the family AtWhy1 and AtWhy3 are imported into plastids while AtWhy2 localizes to mitochondria. Their function in organelles is currently unknown. Results To understand the role of mitochondrial Whirlies in higher plants we produced A. thaliana lines with altered expression of the atwhy2 gene. Organellar DNA immunoprecipitation experiments demonstrated that AtWhy2 binds to mitochondrial .