<> "The repository administrator has not yet configured an RDF license."^^ . <> . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana"^^ . "Na-terminal acetylation (NTA) is one of the most common protein modifications in eukaryotes,\r\ntargeting up to 80% of cytosolic proteins in humans and plants. It is catalyzed by Na-terminal\r\nacetyltransferases (Nats) called NatA-NatH, which transfer the acetyl group from AcetylCoA\r\nto the N-terminus of the substrate proteins. NatA is the major acetyltransferase in eukaryotes,\r\ntargeting up to 50% of proteins in humans and Arabidopsis. In the latter, NTA by NatA is\r\nessential and stabilizes NatA substrates by masking a nonAc-X2/N-degron, which targets\r\nproteins for degradation by the ubiquitin proteasome system. The knockout of NatA leads to\r\nembryo lethality in A.thaliana, while NatA-depleted plants are strongly retarded in growth and\r\nsuffer from enhanced protein turnover. However, they are more resistant to diverse stresses\r\nlike pathogen attack and water limitation, which are sensed by the phytohormones salicylic\r\nacid (SA) and abscisic acid (ABA), respectively.\r\nThe first project of this thesis aimed at identifying biological processes involved in the\r\ngeneration of the dwarf phenotype observed in NatA-depleted mutants. I identified six\r\ncandidate dominant mutations reverting the growth retardation in NatA-depleted mutant\r\nmuse6-1 in a forward genetic screen. One of them was a novel mutation in a pre-mRNA\r\nsplicing machinery which restored the splicing of a mutated auxiliary subunit of NatA, NAA15,\r\nleading to increased NatA levels and restoration of the WT-like phenotype.\r\nThe next part of this work focused on understanding the role of NatA in SA and ABA-triggered\r\nstress responses and dissecting the involvement of the enhanced protein turnover in NatAdepleted\r\nplants for growth retardation under non-stressed conditions and the enhanced\r\nresistance to protein-harming stresses, like water withdrawal.\r\nBy genetic crossing of NatA-depleted plants with mutants impaired in ABA biosynthesis and\r\nsignaling, I demonstrated that the drought resistance of NatA-depleted plants is caused by a\r\nconstitutively activated ABA response upstream of OPEN STOMATA ONE 1 (OST1) but\r\ndownstream of ABA biosynthesis and initial perception. The generation of crosses between\r\nWT Landsberg erecta and the NatA-depleted mutant, muse6-1, disentangled the role of the\r\nconstitutively induced ABA response and upregulated protein turnover in the generation of the\r\ndwarf phenotype in NatA-depleted mutants. WT Ler;muse6-1 crosses partially rescued the\r\nphenotype of NatA-depleted mutants by restoration of WT-like protein turnover rate, albeit the\r\nstomata were still closed. While ABA mediates the stomata closure in NatA-depleted mutants,\r\nit does not contribute to the upregulated protein turnover, which is the major contributor to the\r\ndwarf phenotype of NatA-depleted mutants.\r\nThis thesis disproved the role of the accumulation of yet another phytohormone, SA, in the\r\ngeneration of the dwarf phenotype in NatA-depleted mutants and the upregulation of autophagy\r\nin these lines. However, the higher internal levels of SA in NatA mutants prime the pathogen\r\nresponses in these lines by upregulating the pathogen-response-related genes, yielding them\r\nresistant to H.a. Noco2.\r\nThe depletion of NatA leads to the generation of unstable NatA substrates, which are turned\r\nover at a higher rate by the UPS. In this thesis, I focused on understanding the role of autophagy\r\nin NTA-mediated proteostasis. Various measurements of markers and substrates of autophagy\r\nprovided evidence for its upregulation in NatA-depleted mutants and its role in the turnover of\r\npolyubiquitinated proteins generated upon NatA-depletion. Furthermore, I demonstrated that\r\nNatA-depleted mutants accumulate higher amounts of protein aggregates and that autophagy\r\nis important for surveillance mechanisms in these lines.\r\nIn summary, this thesis highlights the significant role of NTA by NatA in regulating the global\r\nturnover of the proteome, particularly under biotic- and abiotic stresses."^^ . "2024" . . . . . . . "Marlena"^^ . "Pożoga"^^ . "Marlena Pożoga"^^ . . . . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (PDF)"^^ . . . "Thesis_MP_PDFA.pdf"^^ . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (Other)"^^ . . . . . . "indexcodes.txt"^^ . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (Other)"^^ . . . . . . "lightbox.jpg"^^ . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (Other)"^^ . . . . . . "preview.jpg"^^ . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (Other)"^^ . . . . . . "medium.jpg"^^ . . . "Understanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana (Other)"^^ . . . . . . "small.jpg"^^ . . "HTML Summary of #35564 \n\nUnderstanding the stress-induced regulation of Nα-terminal acetylation and its function in the control of proteostasis in Arabidopsis thaliana\n\n" . "text/html" . . . "570 Biowissenschaften, Biologie"@de . "570 Life sciences"@en . .