{"title":"Open field hardening improves leaf physiological drought tolerance in young plants of <i>Sindora siamensis</i>.","authors":"Warunya Paethaisong, Preeyanuch Lakhunthod, Supranee Santanoo, Natthamon Chandarak, Sujittra Onwan, Naruemol Kaewjampa, Anoma Dongsansuk","doi":"10.1071/FP23102","DOIUrl":null,"url":null,"abstract":"<p><p>The effect of drought stress on leaf physiology was studied in 10-month-old plants of Sindora siamensis . Plants were either placed in an open greenhouse (unhardening; UH) or in an open field (open field hardening; H) for 45days. Both the UH and H plants stopped receiving water (D) until the initial drought injury and then rewatered (R) until complete recovery. Results showed necrosis in the leaves of UH+D, while H+D showed wilting at Day 7 after drought. A greater degree of necrosis was found in UH+D+R but made complete recovery in H+D+R at Day 4 after rewatering. Drought stress resulted in decreased leaf area in H, and reduced leaf and stem water status, PSII efficiency, net photosynthetic rate, stomatal conductance and transpiration rate in both UH and H. It also resulted in an increase in water use efficiency in both UH and H. Electrolyte leakage and malondialdehyde contents in UH were markedly increased due to drought stress. These results suggest that unhardened young plants of Sindora exposed to drought exhibited enhanced stomata behaviour by minimising open stomata and transpiration, resulting in high efficiency of water usage. However, there was still membrane damage from lipid peroxidation, which caused necrosis. Open field hardened plants exposed to drought demonstrated reduced open stomata and transpiration, thereby preserving leaf and soil water status and enhancing water use efficiency. This may be a reduction in lipid peroxidation though an oxidative scavenging mechanism that causes a slight alteration in membrane stability and a slight necrosis.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1071/FP23102","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0
Abstract
The effect of drought stress on leaf physiology was studied in 10-month-old plants of Sindora siamensis . Plants were either placed in an open greenhouse (unhardening; UH) or in an open field (open field hardening; H) for 45days. Both the UH and H plants stopped receiving water (D) until the initial drought injury and then rewatered (R) until complete recovery. Results showed necrosis in the leaves of UH+D, while H+D showed wilting at Day 7 after drought. A greater degree of necrosis was found in UH+D+R but made complete recovery in H+D+R at Day 4 after rewatering. Drought stress resulted in decreased leaf area in H, and reduced leaf and stem water status, PSII efficiency, net photosynthetic rate, stomatal conductance and transpiration rate in both UH and H. It also resulted in an increase in water use efficiency in both UH and H. Electrolyte leakage and malondialdehyde contents in UH were markedly increased due to drought stress. These results suggest that unhardened young plants of Sindora exposed to drought exhibited enhanced stomata behaviour by minimising open stomata and transpiration, resulting in high efficiency of water usage. However, there was still membrane damage from lipid peroxidation, which caused necrosis. Open field hardened plants exposed to drought demonstrated reduced open stomata and transpiration, thereby preserving leaf and soil water status and enhancing water use efficiency. This may be a reduction in lipid peroxidation though an oxidative scavenging mechanism that causes a slight alteration in membrane stability and a slight necrosis.