Seed Priming: New Comprehensive Approaches for an Old Empirical Technique

Seed priming is a pre-sowing treatment which leads to a physiological state that enables seed to germinate more efficiently. The majority of seed treatments are based on seed imbibition allowing the seeds to go through the first reversible stage of germination but do not allow radical protrusion through the seed coat. Seeds keeping their desiccation tolerance are then dehydrated and can be stored until final sowing. During subsequent germination, primed seeds exhibit a faster and more synchronized germination and young seedlings are often more vigorous and resistant to abiotic stresses than seedlings obtained from unprimed seeds. Priming often involves soaking seed in predetermined amounts of water or limitation of the imbibition time. The imbibition rate could be somehow controlled by osmotic agents such as PEG and referred as osmopriming. Halopriming implies the use of specific salts while "hormopriming" relies on the use of plant growth regulators. Some physical treatments (UV, cold or heat,..) also provide germination improvement thus suggesting that priming effects are not necessarily related to seed imbibition. A better understanding of the metabolic events taking place during the priming treatment and the subsequent germination should help to use this simple and cheap technology in a more efficient way

PD-L1 Overexpression, SWI/SNF Complex Deregulation, and Profound Transcriptomic Changes Characterize Cancer-Dependent Exhaustion of Persistently Activated CD4+ T Cells

Growing tumors avoid recognition and destruction by the immune system. During continuous stimulation of tumor-infiltrating lymphocytes (TILs) by tumors, TILs become functionally exhausted; thus, they become unable to kill tumor cells and to produce certain cytokines and lose their ability to proliferate. This collectively results in the immune escape of cancer cells. Here, we show that breast cancer cells expressing PD-L1 can accelerate exhaustion of persistently activated human effector CD4+ T cells, manifesting in high PD-1 and PD-L1 expression level son T cell surfaces, decreased glucose metabolism genes, strong downregulation of SWI/SNF chromatin remodelingcomplex subunits, and p21 cell cycle inhibitor upregulation. This results in inhibition of T cell proliferation and reduction of T cell numbers. The RNAseq analysis on exhausted CD4+ T cells indicated strong overexpression of IDO1 and genes encoding pro-inflammatory cytokines and chemokines. Some interleukins were also detected in media from CD4+ T cells co-cultured with cancer cells. The PD-L1 overexpression was also observed in CD4+ T cells after co-cultivation with other cell lines overexpressing PD-L1, which suggested the existence of a general mechanism of CD4+ T cell exhaustion induced by cancer cells. The ChIP analysis on the PD-L1 promoter region indicated that the BRM recruitment in control CD4+ T cells was replaced by BRG1 and EZH2 in CD4+ T cells strongly exhausted by cancer cells. These findings suggest that epi-drugs such as EZH2 inhibitors may be used as immunomodulators in cancer treatment