scholarly journals Rice Na+-Permeable Transporter OsHAK12 Mediates Shoots Na+ Exclusion in Response to Salt Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Linan Zhang ◽  
Xiangyu Sun ◽  
Yanfang Li ◽  
Xuan Luo ◽  
Shaowen Song ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Salt Stress ◽  
Salt Tolerance ◽  
Target Gene ◽  
Xylem Sap ◽  
Crop Productivity ◽  
Membrane Transporter ◽  
High Affinity ◽  
Salt Toxicity ◽  
Plasma Membrane Transporter

Soil salinity has become a major stress factor that reduces crop productivity worldwide. Sodium (Na+) toxicity in a number of crop plants is tightly linked with shoot Na+ overaccumulation, thus Na+ exclusion from shoot is crucial for salt tolerance in crops. In this study, we identified a member of the high-affinity K+ transport family (HAK), OsHAK12, which mediates shoots Na+ exclusion in response to salt stress in rice. The Oshak12 mutants showed sensitivity to salt toxicity and accumulated more Na+ in the xylem sap, leading to excessive Na+ in the shoots and less Na+ in the roots. Unlike typical HAK family transporters that transport K+, OsHAK12 is a Na+-permeable plasma membrane transporter. In addition, OsHAK12 was strongly expressed in the root vascular tissues and induced by salt stress. These findings indicate that OsHAK12 mediates Na+ exclusion from shoot, possibly by retrieving Na+ from xylem vessel thereby reducing Na+ content in the shoots. These findings provide a unique function of a rice HAK family member and provide a potential target gene for improving salt tolerance of rice.

scholarly journals Characterization of Interactions between the Soybean Salt-Stress Responsive Membrane-Intrinsic Proteins GmPIP1 and GmPIP2

Agronomy ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1312
Author(s):  
Jia Liu ◽  
Weicong Qi ◽  
Haiying Lu ◽  
Hongbo Shao ◽  
Dayong Zhang
Keyword(s):  
Plasma Membrane ◽  
Salt Stress ◽  
Salt Tolerance ◽  
Expression Profiles ◽  
Expression Patterns ◽  
Gene Expression Profiles ◽  
Early Gene ◽  
Plant Responses ◽  
Constitutive Overexpression ◽  
Important Trait

Salt tolerance is an important trait in soybean cultivation and breeding. Plant responses to salt stress include physiological and biochemical changes that affect the movement of water across the plasma membrane. Plasma membrane intrinsic proteins (PIPs) localize to the plasma membrane and regulate the water and solutes flow. In this study, quantitative real-time PCR and yeast two-hybridization were engaged to analyze the early gene expression profiles and interactions of a set of soybean PIPs (GmPIPs) in response to salt stress. A total of 20 GmPIPs-encoding genes had varied expression profiles after salt stress. Among them, 13 genes exhibited a downregulated expression pattern, including GmPIP1;6, the constitutive overexpression of which could improve soybean salt tolerance, and its close homologs GmPIP1;7 and 1;5. Three genes showed upregulated patterns, including the GmPIP1;6 close homolog GmPIP1;4, when four genes with earlier increased and then decreased expression patterns. GmPIP1;5 and GmPIP1;6 could both physically interact strongly with GmPIP2;2, GmPIP2;4, GmPIP2;6, GmPIP2;8, GmPIP2;9, GmPIP2;11, and GmPIP2;13. Definite interactions between GmPIP1;6 and GmPIP1;7 were detected and GmPIP2;9 performed homo-interaction. The interactions of GmPIP1;5 with GmPIP2;11 and 2;13, GmPIP1;6 with GmPIP2;9, 2;11 and GmPIP2;13, and GmPIP2;9 with itself were strengthened upon salt stress rather than osmotic stress. Taken together, we inferred that GmPIP1 type and GmPIP2 type could associate with each other to synergistically function in the plant cell; a salt-stress environment could promote part of their interactions. This result provided new clues to further understand the soybean PIP–isoform interactions, which lead to potentially functional homo- and heterotetramers for salt tolerance.

scholarly journals The plasma membrane transporter SLC5A8 suppresses tumour progression through depletion of survivin without involving its transport function

2013 ◽  
Vol 450 (1) ◽  
pp. 169-178 ◽  
Author(s):  
Veena Coothankandaswamy ◽  
Selvakumar Elangovan ◽  
Nagendra Singh ◽  
Puttur D. Prasad ◽  
Muthusamy Thangaraju ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Cancer Cells ◽  
Histone Deacetylase Inhibitors ◽  
Tumour Progression ◽  
Ectopic Expression ◽  
Membrane Transporter ◽  
Transport Function ◽  
Plasma Membrane Transporter

SLC5A8 (solute carrier gene family 5A, member 8) is a sodium-coupled transporter for monocarboxylates. Among its substrates are the HDAC (histone deacetylase) inhibitors butyrate, propionate and pyruvate. Expression of SLC5A8 is silenced in cancers via DNA methylation, and ectopic expression of SLC5A8 in cancer cells induces apoptosis in the presence of its substrates that are HDAC inhibitors. In the present study we show that ectopic expression of SLC5A8 in cancer cells translocates the anti-apoptotic protein survivin to the plasma membrane through protein–protein interaction resulting in depletion of nuclear survivin and also decreases cellular levels of survivin through inhibition of transcription. These SLC5A8-induced changes in the location and levels of survivin result in cell-cycle arrest, disruption of the chromosome passenger complex involved in mitosis, induction of apoptosis and enhancement in chemosensitivity. These effects are seen independently of the transport function of SLC5A8 and histone acetylation status of the cell; in the presence of pyruvate, a SLC5A8 substrate and also an HDAC inhibitor, these effects are amplified. Ectopic expression of SLC5A8 in the breast cancer cell line MB231 inhibits the ability of cells to form colonies in vitro and to form tumours in mouse xenografts in vivo. The suppression of survivin transcription occurs independently of HDAC inhibition, and the underlying mechanism is associated with decreased phosphorylation of STAT3 (signal transducer and activator of transcription 3). The observed effects are specific for survivin with no apparent changes in expression of other inhibitor-of-apoptosis proteins. The present study unravels a novel, hitherto unrecognized, mechanism for the tumour-suppressive role of a plasma membrane transporter independent of its transport function.

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