Project description:High-resolution quantitative profiling of tRNA abundance and modification status in hematopoietic cells upon Trmt6 deletion by mim-tRNAseq
2024-06-03 | GSE252912 | GEO
Project description:Total versus plastidial Mim-tRNAseq
Project description:Measurements of cellular tRNA abundance are hampered by pervasive blocks to cDNA synthesis at modified nucleosides and the extensive similarity among tRNA genes. We overcome these limitations with modification-induced misincorporation tRNA sequencing (mim-tRNAseq), which combines a workflow for full-length cDNA library construction from mature tRNA with a simple-to-use computational analysis toolkit. Our method accurately captures tRNA abundance and modification status in multiple eukaryotes and is applicable to any organism with a known genome.
2021-02-12 | GSE152621 | GEO
Project description:Mim-tRNAseq analysis of wild-type versus mutants affecting tRNA thiolation
Project description:au07-10_mpk - mpk - Gain insight into the function of mpk genes by characterizing the transcriptional profile of the mpk5, mpk10 and mpk11 KO mutants in comparison with that of the Arabidopsis wt plants. - 1) mpk5 (WS genetic background) versus wt-WS 2) mpk11 (Col0 genetic background) versus wt-Col0 3) mpk10 (Col0 genetic background) versus wt-Col0 Seeds were surface sterilized and grown in MS agar medium (3% sucrose) for 11 days in long day conditions. Entire seedling were harvested and deep frozen in liquid nitrogen. Keywords: gene knock out
Project description:Mitochondria play central roles in energetics and metabolism of eukaryotic cells. Their outer membrane is essential for protein transport, membrane dynamics, signalling and metabolic exchange with other cellular compartments. The mitochondrial import complex MIM functions as main translocase for importing the precursors of more than 90% of integral outer membrane proteins. Here we report that the MIM complex performs a second major function in lipid droplet homeostasis. Lipid droplets are crucial in cellular lipid metabolism and as storage organelles for neutral lipids. The lipid metabolism enzyme Ayr1 captures the MIM complex, promoting the formation of mitochondria-lipid droplet contact sites. MIM and Ayr1 enhance the lipid droplet number in cells. Ayr1 binds to MIM via its single hydrophobic segment in a substrate-mimicry mechanisms but remains bound and is not released into the outer membrane. The functional diversity is mediated by different MIM complexes: MIM-Ayr1 for recruiting lipid droplets and MIM-preprotein for protein insertion into the outer membrane. Our work uncovers translocase capture as mechanism for functional conversion of a membrane protein complex from protein insertion to lipid metabolism.
