Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803.
Arsenic is a ubiquitous contaminant and a toxic metalloid which presents two main redox states in nature: arsenite [As(III)] and arsenate [As(V)]. Arsenic resistance in Synechocystis sp. strain PCC 6803 is mediated by the arsBHC operon and two additional arsenate reductases encoded by the arsI1 and...
| Main Authors: | , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2014-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC4010505?pdf=render |
| _version_ | 1819077209367773184 |
|---|---|
| author | Ana María Sánchez-Riego Luis López-Maury Francisco Javier Florencio |
| author_facet | Ana María Sánchez-Riego Luis López-Maury Francisco Javier Florencio |
| author_sort | Ana María Sánchez-Riego |
| collection | DOAJ |
| description | Arsenic is a ubiquitous contaminant and a toxic metalloid which presents two main redox states in nature: arsenite [As(III)] and arsenate [As(V)]. Arsenic resistance in Synechocystis sp. strain PCC 6803 is mediated by the arsBHC operon and two additional arsenate reductases encoded by the arsI1 and arsI2 genes. Here we describe the genome-wide responses to the presence of arsenate and arsenite in wild type and mutants in the arsenic resistance system. Both forms of arsenic produced similar responses in the wild type strain, including induction of several stress related genes and repression of energy generation processes. These responses were transient in the wild type strain but maintained in time in an arsB mutant strain, which lacks the arsenite transporter. In contrast, the responses observed in a strain lacking all arsenate reductases were somewhat different and included lower induction of genes involved in metal homeostasis and Fe-S cluster biogenesis, suggesting that these two processes are targeted by arsenite in the wild type strain. Finally, analysis of the arsR mutant strain revealed that ArsR seems to only control 5 genes in the genome. Furthermore, the arsR mutant strain exhibited hypersentivity to nickel, copper and cadmium and this phenotype was suppressed by mutation in arsB but not in arsC gene suggesting that overexpression of arsB is detrimental in the presence of these metals in the media. |
| first_indexed | 2024-12-21T18:53:34Z |
| format | Article |
| id | doaj.art-03114a56242740d1b82c13c3222f013c |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-21T18:53:34Z |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-03114a56242740d1b82c13c3222f013c2022-12-21T18:53:41ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0195e9682610.1371/journal.pone.0096826Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803.Ana María Sánchez-RiegoLuis López-MauryFrancisco Javier FlorencioArsenic is a ubiquitous contaminant and a toxic metalloid which presents two main redox states in nature: arsenite [As(III)] and arsenate [As(V)]. Arsenic resistance in Synechocystis sp. strain PCC 6803 is mediated by the arsBHC operon and two additional arsenate reductases encoded by the arsI1 and arsI2 genes. Here we describe the genome-wide responses to the presence of arsenate and arsenite in wild type and mutants in the arsenic resistance system. Both forms of arsenic produced similar responses in the wild type strain, including induction of several stress related genes and repression of energy generation processes. These responses were transient in the wild type strain but maintained in time in an arsB mutant strain, which lacks the arsenite transporter. In contrast, the responses observed in a strain lacking all arsenate reductases were somewhat different and included lower induction of genes involved in metal homeostasis and Fe-S cluster biogenesis, suggesting that these two processes are targeted by arsenite in the wild type strain. Finally, analysis of the arsR mutant strain revealed that ArsR seems to only control 5 genes in the genome. Furthermore, the arsR mutant strain exhibited hypersentivity to nickel, copper and cadmium and this phenotype was suppressed by mutation in arsB but not in arsC gene suggesting that overexpression of arsB is detrimental in the presence of these metals in the media.http://europepmc.org/articles/PMC4010505?pdf=render |
| spellingShingle | Ana María Sánchez-Riego Luis López-Maury Francisco Javier Florencio Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. PLoS ONE |
| title | Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. |
| title_full | Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. |
| title_fullStr | Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. |
| title_full_unstemmed | Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. |
| title_short | Genomic responses to arsenic in the cyanobacterium Synechocystis sp. PCC 6803. |
| title_sort | genomic responses to arsenic in the cyanobacterium synechocystis sp pcc 6803 |
| url | http://europepmc.org/articles/PMC4010505?pdf=render |
| work_keys_str_mv | AT anamariasanchezriego genomicresponsestoarsenicinthecyanobacteriumsynechocystissppcc6803 AT luislopezmaury genomicresponsestoarsenicinthecyanobacteriumsynechocystissppcc6803 AT franciscojavierflorencio genomicresponsestoarsenicinthecyanobacteriumsynechocystissppcc6803 |