GRK2-dependent S1PR1 desensitization is required for lymphocytes to overcome their attraction to blood

Lymphocytes egress from lymphoid organs in response to sphingosine-1-phosphate (S1P); minutes later they migrate from blood into tissue against the S1P gradient. The mechanisms facilitating cell movement against the gradient have not been defined. Here, we show that heterotrimeric guanine nucleotide-binding protein-coupled receptor kinase-2 (GRK2) functions in down-regulation of S1P receptor-1 (S1PR1) on blood-exposed lymphocytes. T and B cell movement from blood into lymph nodes is reduced in the absence of GRK2 but is restored in S1P-deficient mice. In the spleen, B cell movement between the blood-rich marginal zone and follicles is disrupted by GRK2 deficiency and by mutation of an S1PR1 desensitization motif. Moreover, delivery of systemic antigen into follicles is impaired. Thus, GRK2-dependent S1PR1 desensitization allows lymphocytes to escape circulatory fluids and migrate into lymphoid tissues.     

Salt tolerance inSolanum kurzianum andS. tuberosum cvs Alpha and Russet Burbank

Summary The cultivated potatoSolanum tuberosum cvs Alpha and Russet Burbank and the wild speciesS. kurzianum were compared with respect to salt tolerance. Plants of the wild species were found to be more salt tolerant than those of the cultivated species since their growth was less impaired by the salinity, although they accumulated more sodium and less potassium ions in the shoot. Unlike the whole plant, callus derived from the wild plants was not more tolerant than that from the cultivated species. Differences in the responses to salinity between cultivated and wild plants, and between the whole plants and calli derived from them are discussed. Based on these differences and the similarity of the physiological responses to salt stress betweenS. kurzianum and the wild salt-tolerant relatives of tomato, the former is suggested as a potential source of genes for increasing the salt tolerance of potato.