Evidence that sulfur metabolism plays a role in microcystin production by Microcystis aeruginosa

Benedict M. Long

doi:10.1016/j.hal.2009.08.003

Evidence that sulfur metabolism plays a role in microcystin production by Microcystis aeruginosa

Benedict M. Long^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

21 Citations (SciVal)

Abstract

Microcystins (MCs) are highly toxic, non-ribosomal cyclic peptides produced by cyanobacteria. A wide range of environmental factors are known to affect MC production, yet the roles these factors play in MC metabolism are poorly understood. In this study a physiological role for sulfur in MC synthesis is proposed. Rates of amino acid and MC-LR production were determined from N-limited chemostat grown cells of the toxic cyanobacterium Microcystis aeruginosa MASH-01A19. Cluster analysis of these rates indicated a correlation between the rates of methionine and MC-LR production, suggesting that a competitive physiological requirement for this sulfur-containing metabolite may limit MC-LR production in this organism. In support of this hypothesis, sulfur limitation in batch cultures led to an approximate 1.5-fold decrease in the intracellular MC-LR quota (Q_MC) over the entire growth cycle, revealing a requirement for sulfur in MC production and suggesting that metabolic demand for methionine may limit MC synthesis. Crown

Original language	English
Pages (from-to)	74-81
Number of pages	8
Journal	Harmful Algae
Volume	9
Issue number	1
DOIs	https://doi.org/10.1016/j.hal.2009.08.003
Publication status	Published - Jan 2010

Access to Document

10.1016/j.hal.2009.08.003

Cite this

@article{13a3dbe6a0cf4ce5996bc207d576a46a,

title = "Evidence that sulfur metabolism plays a role in microcystin production by Microcystis aeruginosa",

abstract = "Microcystins (MCs) are highly toxic, non-ribosomal cyclic peptides produced by cyanobacteria. A wide range of environmental factors are known to affect MC production, yet the roles these factors play in MC metabolism are poorly understood. In this study a physiological role for sulfur in MC synthesis is proposed. Rates of amino acid and MC-LR production were determined from N-limited chemostat grown cells of the toxic cyanobacterium Microcystis aeruginosa MASH-01A19. Cluster analysis of these rates indicated a correlation between the rates of methionine and MC-LR production, suggesting that a competitive physiological requirement for this sulfur-containing metabolite may limit MC-LR production in this organism. In support of this hypothesis, sulfur limitation in batch cultures led to an approximate 1.5-fold decrease in the intracellular MC-LR quota (QMC) over the entire growth cycle, revealing a requirement for sulfur in MC production and suggesting that metabolic demand for methionine may limit MC synthesis. Crown",

keywords = "Amino acids, Batch culture, Chemostat culture, Cluster analysis, Cyanobacteria, Metabolism, Microcystin production, Microcystis aeruginosa, Sulfur",

author = "Long, \{Benedict M.\}",

year = "2010",

month = jan,

doi = "10.1016/j.hal.2009.08.003",

language = "English",

volume = "9",

pages = "74--81",

journal = "Harmful Algae",

issn = "1568-9883",

publisher = "Elsevier B.V.",

number = "1",

}

TY - JOUR

T1 - Evidence that sulfur metabolism plays a role in microcystin production by Microcystis aeruginosa

AU - Long, Benedict M.

PY - 2010/1

Y1 - 2010/1

N2 - Microcystins (MCs) are highly toxic, non-ribosomal cyclic peptides produced by cyanobacteria. A wide range of environmental factors are known to affect MC production, yet the roles these factors play in MC metabolism are poorly understood. In this study a physiological role for sulfur in MC synthesis is proposed. Rates of amino acid and MC-LR production were determined from N-limited chemostat grown cells of the toxic cyanobacterium Microcystis aeruginosa MASH-01A19. Cluster analysis of these rates indicated a correlation between the rates of methionine and MC-LR production, suggesting that a competitive physiological requirement for this sulfur-containing metabolite may limit MC-LR production in this organism. In support of this hypothesis, sulfur limitation in batch cultures led to an approximate 1.5-fold decrease in the intracellular MC-LR quota (QMC) over the entire growth cycle, revealing a requirement for sulfur in MC production and suggesting that metabolic demand for methionine may limit MC synthesis. Crown

AB - Microcystins (MCs) are highly toxic, non-ribosomal cyclic peptides produced by cyanobacteria. A wide range of environmental factors are known to affect MC production, yet the roles these factors play in MC metabolism are poorly understood. In this study a physiological role for sulfur in MC synthesis is proposed. Rates of amino acid and MC-LR production were determined from N-limited chemostat grown cells of the toxic cyanobacterium Microcystis aeruginosa MASH-01A19. Cluster analysis of these rates indicated a correlation between the rates of methionine and MC-LR production, suggesting that a competitive physiological requirement for this sulfur-containing metabolite may limit MC-LR production in this organism. In support of this hypothesis, sulfur limitation in batch cultures led to an approximate 1.5-fold decrease in the intracellular MC-LR quota (QMC) over the entire growth cycle, revealing a requirement for sulfur in MC production and suggesting that metabolic demand for methionine may limit MC synthesis. Crown

KW - Amino acids

KW - Batch culture

KW - Chemostat culture

KW - Cluster analysis

KW - Cyanobacteria

KW - Metabolism

KW - Microcystin production

KW - Microcystis aeruginosa

KW - Sulfur

UR - http://www.scopus.com/inward/record.url?scp=70449520179&partnerID=8YFLogxK

U2 - 10.1016/j.hal.2009.08.003

DO - 10.1016/j.hal.2009.08.003

M3 - Article

SN - 1568-9883

VL - 9

SP - 74

EP - 81

JO - Harmful Algae

JF - Harmful Algae

IS - 1

ER -

Evidence that sulfur metabolism plays a role in microcystin production by Microcystis aeruginosa

Abstract

Access to Document

Other files and links

Fingerprint

Cite this