Background: It is well known that salt stress has different effects on old and young tissues. However, it remains largely unexplored whether old and young tissues have different regulatory mechanism during adaptation of plants to salt stress. The aim of this study was to investigate whether salt stress has different effects on the ion balance and nitrogen metabolism in the old and young leaves of rice, and to compare functions of both organs in rice salt tolerance.
Results: Rice protected young leaves from ion harm via the large accumulation of Na+ and Cl- in old leaves. The up-regulation of OsHKT1;1, OsHAK10 and OsHAK16 might contribute to accumulation of Na+ in old leaves under salt stress. In addition, lower expression of OsHKT1;5 and OsSOS1 in old leaves may decrease frequency of retrieving Na+ from old leaf cells. Under salt stress, old leaves showed higher concentration of NO3- content than young leaves. Up-regulation of OsNRT1;2, a gene coding nitrate transporter, might contribute to the accumulation of NO3- in the old leaves of salt stressed-rice. Salt stress clearly up-regulated the expression of OsGDH2 and OsGDH3 in old leaves, while strongly down-regulated expression of OsGS2 and OsFd-GOGAT in old leaves.
Conclusions: The down-regulation of OsGS2 and OsFd-GOGAT in old leaves might be a harmful response to excesses of Na+ and Cl-. Under salt stress, rice might accumulate Na+ and Cl- to toxic levels in old leaves. This might influence photorespiration process, reduce NH4+ production from photorespiration, and immediately down-regulate the expression of OsGS2 and OsFd-GOGAT in old leaves of salt stressed rice. Excesses of Na+ and Cl- also might change the pathway of NH4+ assimilation in old leaves of salt stressed rice plants, weaken GOGAT/GS pathway and elevate GDH pathway.
背景：鹽脅迫對(duì)老組織和嫩組織具有不同的影響。但是老、嫩組織是否存在不同的鹽脅迫適應(yīng)調(diào)節(jié)機(jī)制還不清楚。本研究的目的是探明鹽脅迫是否在水稻老葉和新葉中對(duì)離子平衡以及氮代謝發(fā)揮不同作用，同時(shí)比較不同組織在鹽脅迫中發(fā)揮的作用。
結(jié)果：水稻通過在老葉中大量積累Na+和Cl-保護(hù)幼葉免于離子毒害。老葉中OsHKT1;1、OsHAK10以及OsHAK16的上調(diào)可能有助于鹽脅迫時(shí)老葉中Na+的積累。此外，OsHKT1;5和OsSOS1在老葉中的低表達(dá)可能降低了從老葉細(xì)胞中的Na+補(bǔ)償。在鹽脅迫下，老葉中NO3-濃度較之幼葉更高。編碼硝酸鹽轉(zhuǎn)運(yùn)蛋白的OsNTR1;2基因在鹽脅迫時(shí)表達(dá)上調(diào)，這可能有助于No3-在老葉中的積累。鹽脅迫顯著上調(diào)OsGDH2和OsGDH3在老葉中表達(dá)上調(diào)，而強(qiáng)烈抑制OsGS2和OsFd-GOGAT在老葉中的表達(dá)。
結(jié)論：OsGS2和OsFd-GOGAT在老葉中的下調(diào)可能是對(duì)Na+、Cl-過量的一種有害應(yīng)答。鹽脅迫下水稻在老葉中積累到有毒害水平的Na+和Cl-。這可能會(huì)影響光呼吸過程，降低光呼吸中NH4+的產(chǎn)生，進(jìn)而鹽脅迫下調(diào)水稻OsGS2和OsFd-GOGAT在老葉中的表達(dá)。鹽脅迫水稻中Na+和Cl-的過量積累也可能改變了老葉中NH4+的同化通路，減弱了GOGAT/GS通路而強(qiáng)化了GDH通路。