fldA is an essential gene required in the 2- C-methyl- D-erythritol 4-phosphate pathway for isoprenoid biosynthesis

Kia-Joo Puan; Hong Wang; Tohru Dairi; Tomohisa Kuzuyama; Craig T Morita

doi:10.1016/j.febslet.2005.05.047

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fldA is an essential gene required in the 2- C-methyl- D-erythritol 4-phosphate pathway for isoprenoid biosynthesis

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fldA is an essential gene required in the 2- C-methyl- D-erythritol 4-phosphate pathway for isoprenoid biosynthesis

Kia-Joo Puan, Hong Wang, Tohru Dairi, Tomohisa Kuzuyama and Craig T Morita

FEBS letters, Vol.579(17), pp.3802-3806

2005

DOI: 10.1016/j.febslet.2005.05.047

PMID: 15978585

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Abstract

Although flavodoxin I is indispensable for Escherichia coli growth, the exact pathway(s) where flavodoxin I is essential has not been identified. We performed transposon mutagenesis of the flavodoxin I gene, fldA, in an E. coli strain that expressed mevalonate pathway enzymes and that had a point mutation in the lytB gene of the MEP pathway resulting in the accumulation of ( E)-4-hydroxy-3-methylbutyl-2-enyl pyrophosphate (HMBPP). Disruption of fldA abrogated mevalonate-independent growth and dramatically decreased HMBPP levels. The fldA − mutant grew with mevalonate indicating that the essential role of flavodoxin I under aerobic conditions is in the MEP pathway. Growth was restored by fldA complementation. Since GcpE (which synthesizes HMBPP) and LytB are iron–sulfur enzymes that require a reducing system for their activity, we propose that flavodoxin is essential for GcpE and possibly LytB activity. Thus, the essential role for flavodoxin I in E. coli is in the MEP pathway for isoprenoid biosynthesis.

2- C-Methyl- D-erythritol 4-phosphate

( E)-4-Hydroxy-3-methylbutyl-2-enyl pyrophosphate

Flavodoxin I

fldA

γδ T cell

Details

Title: Subtitle: fldA is an essential gene required in the 2- C-methyl- D-erythritol 4-phosphate pathway for isoprenoid biosynthesis
Creators: Kia-Joo Puan - Division of Rheumatology, Department of Internal Medicine and the Interdisciplinary Group in Immunology, University of Iowa, EMRB 340F, Iowa City, IA 52242, USA
Hong Wang - Division of Rheumatology, Department of Internal Medicine and the Interdisciplinary Group in Immunology, University of Iowa, EMRB 340F, Iowa City, IA 52242, USA
Tohru Dairi - Biotechnology Research Center, Toyama Prefectural University, Toyama 939-0398, Japan
Tomohisa Kuzuyama - Biotechnology Research Center, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
Craig T Morita - Division of Rheumatology, Department of Internal Medicine and the Interdisciplinary Group in Immunology, University of Iowa, EMRB 340F, Iowa City, IA 52242, USA
Resource Type: Journal article
Publication Details: FEBS letters, Vol.579(17), pp.3802-3806
DOI: 10.1016/j.febslet.2005.05.047
PMID: 15978585
NLM abbreviation: FEBS Lett
ISSN: 0014-5793
eISSN: 1873-3468
Publisher: Elsevier B.V
Language: English
Date published: 2005
Academic Unit: Immunology; Internal Medicine
Record Identifier: 9984094703302771

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