@article {Lytvyn111484, author = {Dmytro I. Lytvyn and Alla I. Yemets and Yaroslav B. Blume}, title = {α-tubulin acetylation and detyrosination correlate with starvation-induced autophagy in tobacco cells}, elocation-id = {111484}, year = {2017}, doi = {10.1101/111484}, publisher = {Cold Spring Harbor Laboratory}, abstract = {Recent data has enabled discovery of novel functions of microtubules (MTs) in the regulation of autophagy development under physiologic/stressful conditions in yeast and animal cells. MTs participate in maturation and traffic of autophagosomes through their dynamic state changes and post-translational modifications of tubulin, including acetylation. We demonstrated the involvement of tobacco cell MTs in the development of starvation-induced autophagy via tubulin acetylation and denitrotyrosination. Induced metabolic stress caused by prolonged cultivation of BY-2 suspension cells results in glucose depletion in the culture medium and following increased rates of protein hydrolysis and autophagy. Development of autophagy was strongly accompanied by α-tubulin acetylation and detyrosination. Both post-translational modifications were caused by changes in the molecular microenvironment of the tobacco cell MTs that was revealed via Co-IP assay. The termination of autophagy led to the development of programmed cell death that was characterised by nucleosomal DNA fragmentation and decreases in α-tubulin acetylation and detyrosination. Our data suggest the role of the functional state of MTs in the mediation of plant autophagy via changes in the tubulin microenvironment and in its post-translational modifications.SUMMARY STATEMENT The main findings cover a possible impact of plant microtubular cytoskeleton to starvation-induced autophagy development. It can be realized by means of tubulin post-translational modifications, acetylation in the first place.MTmicrotubulesTUNELterminal deoxynucleotidyl transferase dUTP nick end labelingPIpropidium iodideDAPI4,6-diamidino-2-phenylindoleMDCMonodansylcadaverineAOacridine orange (AO)}, URL = {https://www.biorxiv.org/content/early/2017/02/24/111484}, eprint = {https://www.biorxiv.org/content/early/2017/02/24/111484.full.pdf}, journal = {bioRxiv} }