Localization of Lipid Droplets in Embryonic Axis Radicle Cells of Soybean Seeds under Various Imbibition Regimes Indicates Their Role in Desiccation Tolerance

Desiccation tolerance allows plant seeds to remain viable during desiccation and subsequent re-hydration. In this study, we tried to develop an experimental system to understand the difference between desiccation tolerant and desiccation sensitive radicle cells by examining excised embryonic axes after re-desiccation and subsequent imbibition under various regimes. Embryonic axes excised from soybean (Glycine max (L.) Merr.) seeds imbibed for 3 h to 15 h which remained attached to the cotyledons during imbibition would grow normally after 24 h of desiccation and re-imbibition on wet filter paper. By contrast, when the embryonic axes excised after 3 h imbibition of seeds were kept on wet filter paper for 12 h to 16 h, their growth was significantly retarded after 24 h of desiccation and subsequent re-imbibition. Numerous lipid droplets were observed lining the plasma membrane and tonoplasts in radicle cells of desiccation tolerant embryonic axes before and after desiccation treatment. By contrast, the lipid droplets lining the plasma membrane and tonoplasts became very sparse in radicle cells that were placed for longer times on wet filter paper before desiccation. We observed a clear correlation between the amount of lipid droplets lining plasma membranes and the ability to grow after desiccation and re-imbibition of the excised embryonic axes. In addition to the reduction of lipid droplets in the cells, a gradual increase in starch grains was observed. Large starch grains accumulated in the radicle cells of those axes that failed to grow further

Localization of Lipid Droplets in Embryonic Axis Radicle Cells of Soybean Seeds under Various Imbibition Regimes Indicates Their Role in Desiccation Tolerance

Desiccation tolerance allows plant seeds to remain viable during desiccation and subsequent re-hydration. In this study, we tried to develop an experimental system to understand the difference between desiccation tolerant and desiccation sensitive radicle cells by examining excised embryonic axes after re-desiccation and subsequent imbibition under various regimes. Embryonic axes excised from soybean (Glycine max (L.) Merr.) seeds imbibed for 3 h to 15 h which remained attached to the cotyledons during imbibition would grow normally after 24 h of desiccation and re-imbibition on wet filter paper. By contrast, when the embryonic axes excised after 3 h imbibition of seeds were kept on wet filter paper for 12 h to 16 h, their growth was significantly retarded after 24 h of desiccation and subsequent re-imbibition. Numerous lipid droplets were observed lining the plasma membrane and tonoplasts in radicle cells of desiccation tolerant embryonic axes before and after desiccation treatment. By contrast, the lipid droplets lining the plasma membrane and tonoplasts became very sparse in radicle cells that were placed for longer times on wet filter paper before desiccation. We observed a clear correlation between the amount of lipid droplets lining plasma membranes and the ability to grow after desiccation and re-imbibition of the excised embryonic axes. In addition to the reduction of lipid droplets in the cells, a gradual increase in starch grains was observed. Large starch grains accumulated in the radicle cells of those axes that failed to grow further

Deficiency of schnurri-2, an MHC enhancer binding protein, induces mild chronic inflammation in the brain and confers molecular, neuronal, and behavioral phenotypes related to schizophrenia.

Schnurri-2 (Shn-2), an nuclear factor-κB site-binding protein, tightly binds to the enhancers of major histocompatibility complex class I genes and inflammatory cytokines, which have been shown to harbor common variant single-nucleotide polymorphisms associated with schizophrenia. Although genes related to immunity are implicated in schizophrenia, there has been no study showing that their mutation or knockout (KO) results in schizophrenia. Here, we show that Shn-2 KO mice have behavioral abnormalities that resemble those of schizophrenics. The mutant brain demonstrated multiple schizophrenia-related phenotypes, including transcriptome/proteome changes similar to those of postmortem schizophrenia patients, decreased parvalbumin and GAD67 levels, increased theta power on electroencephalograms, and a thinner cortex. Dentate gyrus granule cells failed to mature in mutants, a previously proposed endophenotype of schizophrenia. Shn-2 KO mice also exhibited mild chronic inflammation of the brain, as evidenced by increased inflammation markers (including GFAP and NADH/NADPH oxidase p22 phox), and genome-wide gene expression patterns similar to various inflammatory conditions. Chronic administration of anti-inflammatory drugs reduced hippocampal GFAP expression, and reversed deficits in working memory and nest-building behaviors in Shn-2 KO mice. These results suggest that genetically induced changes in immune system can be a predisposing factor in schizophrenia