Modulation of cellular redox status by thiamine-activated NADPH oxidase confers Arabidopsis resistance to Sclerotinia sclerotiorum
Sclerotinia sclerotiorum can initially suppress host oxidative burst to aid infection establishment, but later promotes reactive oxygen species (ROS) generation as proliferation advances. Here, it was shown that the cellular redox status can be modulated by thiamine to protect Arabidopsis thaliana against Sclerotinia at the early stages of infection. The initial inhibition of host ROS generation by Sclerotinia-secreted oxalate could effectively be alleviated by thiamine. Thiamine pre-treatment and subsequent wild-type Sclerotinia invasion induced an increase of ascorbate peroxidase activity concomitant with decreased ascorbate/dehydroascorbate ratios, which led to the cellular transition towards oxidative status in infected tissues. Particularly, it was observed that wild-type Sclerotinia, but not oxalate-deficient A2 mutant, could suppress the activity of NADPH oxidase (NOX), which might be an important mechanism underlying the early inhibition of ROS burst. Nevertheless, thiamine pre-treatment followed by wild-type Sclerotinia infection promoted NOX-derived ROS accumulation. Further studies showed that cytosolic Ca(2+) and staurosporine-sensitive protein kinase(s) participated in thiamine-induced activation of NOX. Moreover, thiamine-induced tissue defence responses including callose/lignin deposition and stomatal closure were closely correlated with NOX-derived ROS generation. Additionally, studies with Brassica species indicated that the regulation of thiamine is largely conserved upon Sclerotinia infection. Collectively, it was concluded that thiamine reverses the initial reducing status through activating NOX-dependent ROS signalling to perturb the disease progress of Sclerotinia.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2013 |
|---|---|
| Erschienen: |
2013 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:64 |
|---|---|
| Enthalten in: |
Journal of experimental botany - 64(2013), 11 vom: 01. Aug., Seite 3261-72 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Zhou, Jun [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Callose |
|---|
| Anmerkungen: |
Date Completed 22.10.2013 Date Revised 16.11.2017 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1093/jxb/ert166 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM228782422 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM228782422 | ||
| 003 | DE-627 | ||
| 005 | 20231224080713.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231224s2013 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1093/jxb/ert166 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0762.xml |
| 035 | |a (DE-627)NLM228782422 | ||
| 035 | |a (NLM)23814275 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Zhou, Jun |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Modulation of cellular redox status by thiamine-activated NADPH oxidase confers Arabidopsis resistance to Sclerotinia sclerotiorum |
| 264 | 1 | |c 2013 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 22.10.2013 | ||
| 500 | |a Date Revised 16.11.2017 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Sclerotinia sclerotiorum can initially suppress host oxidative burst to aid infection establishment, but later promotes reactive oxygen species (ROS) generation as proliferation advances. Here, it was shown that the cellular redox status can be modulated by thiamine to protect Arabidopsis thaliana against Sclerotinia at the early stages of infection. The initial inhibition of host ROS generation by Sclerotinia-secreted oxalate could effectively be alleviated by thiamine. Thiamine pre-treatment and subsequent wild-type Sclerotinia invasion induced an increase of ascorbate peroxidase activity concomitant with decreased ascorbate/dehydroascorbate ratios, which led to the cellular transition towards oxidative status in infected tissues. Particularly, it was observed that wild-type Sclerotinia, but not oxalate-deficient A2 mutant, could suppress the activity of NADPH oxidase (NOX), which might be an important mechanism underlying the early inhibition of ROS burst. Nevertheless, thiamine pre-treatment followed by wild-type Sclerotinia infection promoted NOX-derived ROS accumulation. Further studies showed that cytosolic Ca(2+) and staurosporine-sensitive protein kinase(s) participated in thiamine-induced activation of NOX. Moreover, thiamine-induced tissue defence responses including callose/lignin deposition and stomatal closure were closely correlated with NOX-derived ROS generation. Additionally, studies with Brassica species indicated that the regulation of thiamine is largely conserved upon Sclerotinia infection. Collectively, it was concluded that thiamine reverses the initial reducing status through activating NOX-dependent ROS signalling to perturb the disease progress of Sclerotinia | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Callose | |
| 650 | 4 | |a NADPH oxidase | |
| 650 | 4 | |a Sclerotinia | |
| 650 | 4 | |a oxalate | |
| 650 | 4 | |a redox status | |
| 650 | 4 | |a thiamine. | |
| 650 | 7 | |a NADPH Oxidases |2 NLM | |
| 650 | 7 | |a EC 1.6.3.- |2 NLM | |
| 650 | 7 | |a Thiamine |2 NLM | |
| 650 | 7 | |a X66NSO3N35 |2 NLM | |
| 700 | 1 | |a Sun, Aizhen |e verfasserin |4 aut | |
| 700 | 1 | |a Xing, Da |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of experimental botany |d 1985 |g 64(2013), 11 vom: 01. Aug., Seite 3261-72 |w (DE-627)NLM098182706 |x 1460-2431 |7 nnns |
| 773 | 1 | 8 | |g volume:64 |g year:2013 |g number:11 |g day:01 |g month:08 |g pages:3261-72 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1093/jxb/ert166 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 64 |j 2013 |e 11 |b 01 |c 08 |h 3261-72 | ||