Project description:Background: Rice is a staple crop for over half of the global population, but soil salinization poses a significant threat to its production. As a type of polyamine, spermidine (Spd) has been shown to reduce stress-induced damage in plants, but its specific role and mechanism in protecting rice roots under salt stress require further investigation. Results: This study suggested spermidine (Spd) mitigates salt stress on rice root growth by enhancing antioxidant enzyme activity and reducing peroxide levels. Transcriptomic analysis showed that salt stress caused 333 genes to be upregulated and 1,765 to be downregulated. However, adding Spd during salt treatment significantly altered this pattern: 2,298 genes were upregulated and 844 were downregulated, which indicated Spd reverses some transcriptional changes caused by salt stress. KEGG pathway analysis suggested that Spd influenced key signaling pathways, including MAPK signaling, plant hormone signal transduction, and phenylalanine metabolism. Additionally, the bZIP transcription factor OsbZIP73 was upregulated after Spd treatment, which is confirmed by Western blot. Further insights into the interaction between OsbZIP73 and Spd were gained through fluorescence polarization experiments, showing that Spd enhances protein OsbZIP73's affinity for RNA. Functional enrichment analyses revealed that OsPYL1, OsSPARK1, and various SAUR family genes involved in Spd-affected pathways. The presence of G/A/C-box elements in these genes suggests they are potential targets for OsbZIP73. Conclusions: Our findings suggest a strategy of using spermidine as a chemical alleviator for salt stress and provide insights into the regulatory function of OsbZIP73 in mitigating salt stress in rice roots.
2024-08-01 | GSE189665 | GEO
Project description:WES of dentinogenesis imperfecta family
| PRJNA1066209 | ENA
Project description:WES of dentinogenesis imperfecta family
| PRJNA954345 | ENA
Project description:WES of amelogenesis imperfecta family
Project description:Spermidine (SPD), a polyamine naturally present in living organisms, is known to prolong lifespan in animals. In this study, the role of SPD in melanogenesis were investigated and showed the possibility as a pigmenting agent. SPD treatment increased melanin production in melanocytes in a dose dependent manner. Computational analysis with RNA-sequencing data revealed the alteration of protein degradation by SPD treatment without changing the expressions of melanogenesis-related genes. Indeed, SPD treatment significantly increased the stabilities of tyrosinase-related protein (TRP)-1 and -2 while inhibiting ubiquitination, which was confirmed by treatment of proteasome inhibitor MG132. Inhibition of protein synthesis by cycloheximide (CHX) showed that SPD treatment increased the resistance of TRP-1 and TRP-2 to protein degradation. To identify the proteins involved in SPD transportation in melanocytes, the expression of several solute carrier (SLC) membrane transporters was assessed and, among 27 transporter genes, SLC3A2, SLC7A1, SLC18B1, and SLC22A18 were highly expressed, implying they are putative SPD transporters in melanocytes. Furthermore, SLC7A1 and SLC22A18 were downregulated by SPD treatment, indicating their active involvement in polyamine homeostasis. Finally, we applied SPD to a human skin equivalent and observed elevated melanin production. Our results identify SPD as a potential natural product to alleviate hypopigmentation.
Project description:In this study, we investigated the transcriptomic response of Streptococcus pneumoniae D39 to methionine. Transcriptome comparison of the S. pneumoniae D39 wild-type grown in chemically defined medium (CDM) with 0mM to 10mM methionine revealed the elevated expression of various genes/operons involved in methionine synthesis and transport (fhs, folD, gshT, metA, metB, metEF, metQ, tcyB, spd-0150, spd-0431, and spd-0618). We further demonstrated by β-galactosidase assays and quantitative RT-PCR studies that the transcriptional regulator, CmhR (SPD-0588) acts as a transcriptional activator of the fhs, folD, metB, metEF, metQ, and spd-0431 genes. We identified a putative regulatory site of CmhR in the promoter region of CmhR regulated genes and this CmhR site was further confirmed by promoter mutational experiments.
2016-10-15 | GSE88766 | GEO
Project description:WES sequecning of AI family in China
| PRJNA1184796 | ENA
Project description:WES data for bilateral renal agenesis family
Project description:Potocki-Shaffer syndrome (PSS) is a rare contiguous gene deletion syndrome marked by haploinsufficiency of genes in chromosomal region 11p11.2p12. Approximately 50 cases of PSS have been reported; however, a syndrome with a PSS-like clinical phenotype caused by 11p11.12p12 duplication has not yet been reported. We first report the 11p11.12p12 duplication in a family with intellectual disability and craniofacial anomalies. 11p11.12p12 duplication syndrome was identified by karyotype analysis. Next-generation sequencing (NGS) analysis clarified the location of the chromosomal variations, which was confirmed by chromosome microarray analysis (CMA). Whole-exome sequencing (WES) was performed to exclude single nucleotide variations (SNVs). The raw data of NGS analysis and WES have been submitted to SRA, the accession number is PRJNA713823.
Project description:To uncover the mechanism of SPD-induced autophagy in FGSCs, we used RNA sequencing technology to compare the mRNA expression differences between the control groups and the SPD treated groups. FGSCs mRNA profiles of the control groups and the SPD treated groups were generated by deep sequencing, in two replicates. The library quality was determined using a Bioanalyzer 2100 (Agilent). The Illumina HiSeq 2500 platform was used for RNA sequencing. The quality of RNA-seq reads was examined using FastQC.