@article{YangPerreraSaplaouraetal.2019,
  author    = {Yang, Lei and Perrera, Valentina and Saplaoura, Eleftheria and Apelt, Federico and Bahin, Mathieu and Kramdi, Amira and Olas, Justyna Jadwiga and M{\"u}ller-R{\"o}ber, Bernd and Sokolowska, Ewelina and Zhang, Wenna and Li, Runsheng and Pitzalis, Nicolas and Heinlein, Manfred and Zhang, Shoudong and Genovesio, Auguste and Colot, Vincent and Kragler, Friedrich},
  title     = {m(5)C Methylation Guides Systemic Transport of Messenger RNA over Graft Junctions in Plants},
  series = {Current biology},
  volume    = {29},
  journal   = {Current biology},
  number    = {15},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {0960-9822},
  doi       = {10.1016/j.cub.2019.06.042},
  pages     = {2465 -- 2476.e5},
  year      = {2019},
  abstract  = {In plants, transcripts move to distant body parts to potentially act as systemic signals regulating development and growth. Thousands of messenger RNAs (mRNAs) are transported across graft junctions via the phloem to distinct plant parts. Little is known regarding features, structural motifs, and potential base modifications of transported transcripts and how these may affect their mobility. We identified Arabidopsis thalianam RNAs harboring the modified base 5-methylcytosine (m(5)C) and found that these are significantly enriched in mRNAs previously described as mobile, moving over graft junctions to distinct plant parts. We confirm this finding with graft-mobile methylated mRNAs TRANSLATIONALLY CONTROLLED TUMOR PROTEIN 1 (TCTP1) and HEAT SHOCK COGNATE PROTEIN 70.1 (HSC70.1), whose mRNA transport is diminished in mutants deficient in m(5)C mRNA methylation. Together, our results point toward an essential role of cytosine methylation in systemic mRNA mobility in plants and that TCTP1 mRNA mobility is required for its signaling function.},
  language  = {en}
}
@article{FriedrichOberkoflerTrindadeetal.2021,
  author    = {Friedrich, Thomas and Oberkofler, Vicky and Trindade, In{\^e}s and Altmann, Simone and Brzezinka, Krzysztof and L{\"a}mke, J{\"o}rn S. and Gorka, Michal and Kappel, Christian and Sokolowska, Ewelina and Skirycz, Aleksandra and Graf, Alexander and B{\"a}urle, Isabel},
  title     = {Heteromeric HSFA2/HSFA3 complexes drive transcriptional memory after heat stress in Arabidopsis},
  series = {Nature Communications},
  volume    = {12},
  journal   = {Nature Communications},
  number    = {1},
  publisher = {Nature Publishing Group UK},
  address   = {[London]},
  issn      = {2041-1723},
  doi       = {10.1038/s41467-021-23786-6},
  pages     = {15},
  year      = {2021},
  abstract  = {Adaptive plasticity in stress responses is a key element of plant survival strategies. For instance, moderate heat stress (HS) primes a plant to acquire thermotolerance, which allows subsequent survival of more severe HS conditions. Acquired thermotolerance is actively maintained over several days (HS memory) and involves the sustained induction of memory-related genes. Here we show that FORGETTER3/ HEAT SHOCK TRANSCRIPTION FACTOR A3 (FGT3/HSFA3) is specifically required for physiological HS memory and maintaining high memory-gene expression during the days following a HS exposure. HSFA3 mediates HS memory by direct transcriptional activation of memory-related genes after return to normal growth temperatures. HSFA3 binds HSFA2, and in vivo both proteins form heteromeric complexes with additional HSFs. Our results indicate that only complexes containing both HSFA2 and HSFA3 efficiently promote transcriptional memory by positively influencing histone H3 lysine 4 (H3K4) hyper-methylation. In summary, our work defines the major HSF complex controlling transcriptional memory and elucidates the in vivo dynamics of HSF complexes during somatic stress memory. Moderate heat stress primes plants to acquire tolerance to subsequent, more severe heat stress. Here the authors show that the HSFA3 transcription factor forms a heteromeric complex with HSFA2 to sustain activated transcription of genes required for acquired thermotolerance by promoting H3K4 hyper-methylation.},
  language  = {en}
}