There is large area of saline abandoned and lowyielding land distributed in coastal zone in the world. Soil salinity which inhibits plant growth and decreases crop yield is a serious and chronic problem for agricultural production. Improving plant salt tolerance is a feasible way to solve this problem. Plant physiological and biochemical responses under salinity stress become a hot issue at present, because it can provide insights into how plants may be modified to become more tolerant. It is generally known that the negative effects of soil salinity on plants are ascribed to ion toxicity, oxidative stress and osmotic stress, and great progress has been made in the study on molecular and physiological mechanisms of plant salinity tolerance in recent years. However, the present knowledge is not easily applied in the agronomy research under field environment. In this review, we simplified the physiological adaptive mechanisms in plants grown in saline soil and put forward a practical procedure for discerning physiological status and responses. In our opinion, this procedure consists of two steps. First, negative effects of salt stress are evaluated by the changes in biomass, crop yield and photosynthesis. Second, the underlying reasons are analyzed from osmotic regulation, antioxidant response and ion homeostasis. Photosynthesis is a good indicator of the harmful effects of saline soil on plants because of its close relation with crop yield and high sensitivity to environmental stress. Particularly, chlorophyll a fluorescence transient has been accepted as a reliable, sensitive and convenient tool in photosynthesis research in recent years, and it can facilitate and enrich photosynthetic research under field environment.

Plant photosynthesis and photosystem II (PSII) are susceptible to high temperature. However, photosynthetic electron transport process under heat stress remains unclear. To reveal this issue, chlorophyll a fluorescence and modulated 820 nm reflection were simultaneously detected in sweet sorghum. At 43°C, J step in the chlorophyll a fluorescence transient was significantly elevated, suggesting that electron transport beyond primary quinone of PSII (QA) (primary quinone electron acceptor of PSII) was inhibited. PSI (Photosystem I) photochemical capacity was not influenced even under severe heat stress at 48°C. Thus, PSI oxidation was prolonged and PSI re-reduction did not reach normal level. The inhibition of electron transport between PSII and PSI can reduce the possibility of PSI photoinhibition under heat stress. PSII function recovered entirely one day after heat stress at 43°C, implying that sweet sorghum has certain self-remediation capacity. When the temperature reached 48°C, the maximum quantum yield for primary photochemistry and the electron transport from PSII donor side were remarkably decreased, which greatly limited the electron flow to PSI, and PSI re-reduction suspended. The efficiency of an electron transferred from the intersystem electron carrier (plastoquinol, PQH2) to the end electron acceptors at the PSI acceptor side increased significantly at 48°C, and the reason was the greater inhibition of electron transport before PQH2. Thus, the fragment from QA to PQH2 is the most heat sensitive in the electron transport chain between PSII and PSI in sweet sorghum.

Plants establish mutualistic associations with beneficial microbes while deploying the immune system to defend against pathogenic ones. Little is known about the interplay between mutualism and immunity and the mediator molecules enabling such crosstalk. Here, we show that plants respond differentially to a volatile bacterial compound through integral modulation of the immune system and the phosphate-starvation response (PSR) system, resulting in either mutualism or immunity. We found that exposure of Arabidopsis thaliana to a known plant growth-promoting rhizobacterium can unexpectedly have either beneficial or deleterious effects to plants. The beneficial-to-deleterious transition is dependent on availability of phosphate to the plants and is mediated by diacetyl, a bacterial volatile compound. Under phosphate-sufficient conditions, diacetyl partially suppresses plant production of reactive oxygen species (ROS) and enhances symbiont colonization without compromising disease resistance. Under phosphate-deficient conditions, diacetyl enhances phytohormone-mediated immunity and consequently causes plant hyper-sensitivity to phosphate deficiency. Therefore, diacetyl affects the type of relation between plant hosts and certain rhizobacteria in a way that depends on the plant's phosphate-starvation response system and phytohormone-mediated immunity.