NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis

Chloroplasts generate important cellular signals and synthesize diverse products. The chloroplast-localized protein, Nitric Oxide Associated-1 (NOA1), is implicated in nitric oxide (NO) accumulation and linked to the methylerythritol phosphate (MEP) pathway, but its role is undefined. I report that...

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Other Authors: Braam, Janet
Format: Others
Language:English
Published: 2013
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Online Access:http://hdl.handle.net/1911/70480
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spelling ndltd-RICE-oai-scholarship.rice.edu-1911-704802013-05-01T03:47:47ZNOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in ArabidopsisBiological sciencesPlant biologyChloroplasts generate important cellular signals and synthesize diverse products. The chloroplast-localized protein, Nitric Oxide Associated-1 (NOA1), is implicated in nitric oxide (NO) accumulation and linked to the methylerythritol phosphate (MEP) pathway, but its role is undefined. I report that NOA1 is not essential for NO accumulation because the noa1 mutant accumulates NO when provided sucrose-supplemented media. Therefore, chloroplast function and fixed carbon, but not NOA1 are likely critical for plant NO accumulation. noa1 is also resistant to fosmidomycin, an inhibitor of the MEP pathway. This phenotype led to uncovering a potential link between the MEP and tetrapyrrole pathways. I report that fosmidomycin toxicity is light dependent and reduced by phytol supplementation. Downregulation of the tetrapyrrole pathway enhances fosmidomycin resistance, suggesting that reduced tetrapyrrole biosynthesis alleviates fosmidomycin toxicity. These findings reveal new insight into how impairment of the MEP pathway affects plants and the importance of metabolic balance for chloroplast function.Braam, Janet2013-03-08T00:39:47Z2013-03-08T00:39:47Z2012ThesisText67 p.application/pdfhttp://hdl.handle.net/1911/70480VanReeKeng
collection NDLTD
language English
format Others
sources NDLTD
topic Biological sciences
Plant biology
spellingShingle Biological sciences
Plant biology
NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
description Chloroplasts generate important cellular signals and synthesize diverse products. The chloroplast-localized protein, Nitric Oxide Associated-1 (NOA1), is implicated in nitric oxide (NO) accumulation and linked to the methylerythritol phosphate (MEP) pathway, but its role is undefined. I report that NOA1 is not essential for NO accumulation because the noa1 mutant accumulates NO when provided sucrose-supplemented media. Therefore, chloroplast function and fixed carbon, but not NOA1 are likely critical for plant NO accumulation. noa1 is also resistant to fosmidomycin, an inhibitor of the MEP pathway. This phenotype led to uncovering a potential link between the MEP and tetrapyrrole pathways. I report that fosmidomycin toxicity is light dependent and reduced by phytol supplementation. Downregulation of the tetrapyrrole pathway enhances fosmidomycin resistance, suggesting that reduced tetrapyrrole biosynthesis alleviates fosmidomycin toxicity. These findings reveal new insight into how impairment of the MEP pathway affects plants and the importance of metabolic balance for chloroplast function.
author2 Braam, Janet
author_facet Braam, Janet
title NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
title_short NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
title_full NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
title_fullStr NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
title_full_unstemmed NOA1: A Tool for Understanding Nitric Oxide Accumulation and Fosmidomycin Resistance in Arabidopsis
title_sort noa1: a tool for understanding nitric oxide accumulation and fosmidomycin resistance in arabidopsis
publishDate 2013
url http://hdl.handle.net/1911/70480
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