| dc.creator |
Yamamoto, Yoko |
|
| dc.creator |
Hasezawa, Seiichiro |
|
| dc.creator |
Tsuchiya, Yoshiyuki |
|
| dc.creator |
TÜRKAN, İSMAİL |
|
| dc.creator |
Demiral, Tijen |
|
| dc.creator |
Sano, Toshio |
|
| dc.creator |
Kariya, Koki |
|
| dc.creator |
Sasaki, Takayuki |
|
| dc.date |
2013-11-01T01:00:00Z |
|
| dc.date.accessioned |
2025-02-25T10:22:33Z |
|
| dc.date.available |
2025-02-25T10:22:33Z |
|
| dc.identifier |
5a47f7cb-9b1a-4b8e-ab87-21cd682453a3 |
|
| dc.identifier |
10.1016/j.jinorgbio.2013.07.001 |
|
| dc.identifier |
https://avesis.sdu.edu.tr/publication/details/5a47f7cb-9b1a-4b8e-ab87-21cd682453a3/oai |
|
| dc.identifier.uri |
http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/99826 |
|
| dc.description |
The role of vacuole in the cell death mechanism induced by aluminium (Al) was investigated in tobacco (Nicotiana tabacum L) cell line BY-2. Cells at logarithmic phase of growth were treated without (control) or with Al (up to 150 mu M) in a treatment medium containing CaCl2, sucrose and 2-(N-morpholino) ethanesulfonic acid (MES) buffer (pH 5.0). After 18 h treatment, both the integrity of the plasma membrane (estimated by Evans blue uptake) and growth capacity (estimated by post-Al treatment growth in nutrient medium) were decreased, while the activity of vacuolar processing enzyme (VPE) was increased, in the Al dose-dependent manner. The activity of the vacuole (estimated by neutral red uptake) was slightly increased at 50 mu M then decreased with an increase in Al concentration. Direct observation of morphological changes of vacuole in a transgenic BY-2 expressing GFP-AtVam3p fusion protein localized on tonoplast indicated Al-induced collapse of vacuole. Time-course experiments indicated that both an increase in VPE activity and a loss of growth capacity were clearly observed at 6 h of the treatment time, prior to the loss of plasma membrane integrity. The presence of Ac-YVAD-CHO (an inhibitor effective to VPE) during Al treatment suppressed a loss of plasma membrane integrity. The expression of VPE genes (VPE-1a, VPE-1b) were significantly enhanced by Al treatment Taken together, we conclude that an enhancement of WE activity by Al is controlled at transcriptional level, and is a key factor leading to a loss of integrity of the plasma membrane and a loss of growth capacity. (C) 2013 Elsevier Inc. All rights reserved. |
|
| dc.language |
eng |
|
| dc.rights |
info:eu-repo/semantics/closedAccess |
|
| dc.title |
A novel mechanism of aluminium-induced cell death involving vacuolar processing enzyme and vacuolar collapse in tobacco cell line BY-2 |
|
| dc.type |
info:eu-repo/semantics/article |
|