Deciphering the SUMO code in plants
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ABSTRACT:
PROVIDER: PRJNA1148947 | ENA |
REPOSITORIES: ENA
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Project description:Post-translational modification (PTM) events generate proteoforms that orchestrate cell signalling in almost every biological process. The SUMOcode project aims to understand a critically important but understudied PTM in plants, SUMO (Small Ubiquitin-like Modifier). The rules governing specificity and function remain rudimentary for most PTMs, but the plant SUMO system provides a unique possibility to unravel the rules governing SUMOylation, as its core machinery comprises only 33 genes in Arabidopsis, compared with many hundreds for other PTMs. Our central hypothesis is that SUMO specificity is conferred through how cells are primed to respond to different stress signals, the tissue and cellular spatial distribution of SUMO machinery and substrates and control of SUMOylation modification via activation, repression and competition for PTM sites. Given the small numbers of genes involved in SUMOylation, we are in an excellent position to test our hypothesis employing state of the art multi-omics technologies to create the first SUMO Cell Atlas of any organism. Our ultimate goal is to 'enable' researchers and breeders to decipher the SUMO code in plants, enabling them to edit and rewrite the code, to develop crops that are future proofed against ongoing climate instability and change.
2025-07-21 | GSE275006 | GEO
Project description:Deciphering the reading of the genetic code by near-cognate tRNA
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Project description:Deciphering the ‘m6A code’ via quantitative profiling of m6A at single-nucleotide resolution
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Project description:Deciphering the principles of the RNA editing code via large-scale systematic probing
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Project description:Protein SUMOylation orchestrates diverse cellular processes and is linked to diseases such as cancer and neurodegenerative disorders. However, large-scale identification endogenous SUMO-1 poses challenges due to current enrichment methods limitations and its lower abundance compared to SUMO-2/3. To solve this problem, we developed a series of novel peptide ligands via phage display, specifically targeting the C-terminal region of SUMO-1 remnants. These peptide ligands exhibited robust affinity for SUMO-1 modified peptide segments, facilitating the development of a peptide-based enrichment strategy. Using this strategy, we mapped 1312 SUMOylation sites in HeLa cells, unveiling a comprehensive SUMOylation landscape. We further applied our approach to the Alzheimer's disease (AD) model mice, revealing 1364 SUMOylation sites and 991 endogenous SUMOylation proteins in mice brain tissues. Notably, AD mice brain tissues exhibited significantly elevated SUMO-1 modification levels. Differential protein analysis, including previously unreported SUMOylation substrates, were identified and the reliability of our identification strategy was validated through SUMO-1 modification of ULK2 in AD mice brain tissues by co-immunoprecipitation. This work advances endogenous SUMO-1 proteome, providing insights and potential disease targets, particularly for AD. Moreover, our strategy, bolstered by the utility of phage display technology, opens new avenues for the development of enrichment materials in various other post-translational modifications.
2024-03-18 | PXD050705 |
Project description:Mouse embryonic fibroblasts (MEFs) were generated from Ubc9fl/- and Ubc9+/+ embryos (E13.5). MEFs were treated with tamoxifen for six days to cause CreERT2 activation, and induce Ubc9 floxed allele deletion. We determined the ChIP-seq profiles of SUMO-1 and SUMO-2 using chromatin of wild-type MEFs Ubc9+/+ and of the corresponding Ubc9 KO MEFs which are entirely depleted for sumoylation. The analysis revealed the nearly complete absence of genome-wide binding of SUMO-1 and SUMO-2 in Ubc9-/- MEFs, attesting for antibody specificities.
2018-10-24 | GSE115842 | GEO
Project description:Deciphering the ‘m6A code’ via quantitative profiling of m6A at single-nucleotide resolution [III]
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Project description:Deciphering the ‘m6A code’ via quantitative profiling of m6A at single-nucleotide resolution [I]
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Project description:Deciphering the ‘m6A code’ via quantitative profiling of m6A at single-nucleotide resolution [II]
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Project description:Short periods of heat (>37°C) are extremely damaging to non-acclimated plants and their capacity to acclimate to and recover from heat stress is a key parameter for their survival and longevity. To acclimate, the Heat Shock transcription Factor A1 (HSFA1) subfamily activates a transcriptional response that resolves the heat stress-induced protein damage. Importantly, HSFA1 activity is also critical for Arabidopsis to withstand sustained warmer periods of 28°C, a non-detrimental condition that triggers a thermomorphogenesis response. We find that SUMO, a protein modification whose adduct levels increase as a result of acute heat stress in eukaryotes, is also critical for plant longevity during warmer periods, in particular for shoot meristem development. The known E3 and E4 SUMO ligases (SIZ1, HPY1/MMS21, PIAL1/2) were not essential to endure these warmer periods, alone or in combination. Thermo-lethality was also not seen when plants lacked certain SUMO proteases (ESD4, OTS1/OTS2, SPF1/SPF2 combined) or when SUMO chain formation was blocked. Furthermore, SUMO thermo-resilience is not connected to the autoimmune phenotype found in the corresponding SUMO knockdown and a SIZ1 loss-of-function mutant. As acquired thermotolerance was normal in the SUMO knockdown mutant, we thus conclude that the role of SUMO in heat acclimation differs from that of HSFA1 and SIZ1. Combined, this study reveals that SUMO appears to be critical for shoot meristem integrity during warmer periods. This experiment we have examined how gene expression is affected in two SUMO mutants (siz1-2; sumo1 amiR-SUMO1 [aka. sumo1/2KD] ), and a HsfA1a,b,d triple mutant, when the plants are placed at 28C constant ambient temperature, which is a condition normally used to induce thermomorphogenesis. We used as control the pad1-4 background, as the siz1-2 and sumo1/2KD mutants normally suffer from constitutive defence signalling due hyperaccumulation of SA, which is suppressed by introgression of pad4 in these backgrounds.
2020-08-31 | GSE149122 | GEO