@article{12192,
  abstract     = {Transposable elements (TEs), the movement of which can damage the genome, are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in the sperm companion cell – vegetative cell (VC) – of the flowering plant Arabidopsis thaliana. However, the extent and mechanism of this activation are unknown. Here we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed DNA demethylation. We further demonstrate that DEMETER access to some of these TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent mechanism. We demonstrate that H1 is required for heterochromatin condensation in plant cells and show that H1 overexpression creates heterochromatic foci in the VC progenitor cell. Taken together, our results demonstrate that the natural depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation, heterochromatin relaxation, and TE activation.},
  author       = {He, Shengbo and Vickers, Martin and Zhang, Jingyi and Feng, Xiaoqi},
  issn         = {2050-084X},
  journal      = {eLife},
  keywords     = {General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine, General Neuroscience},
  publisher    = {eLife Sciences Publications, Ltd},
  title        = {{Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation}},
  doi          = {10.7554/elife.42530},
  volume       = {8},
  year         = {2019},
}

@article{10370,
  abstract     = {Eukaryotic cells are densely packed with macromolecular complexes and intertwining organelles, continually transported and reshaped. Intriguingly, organelles avoid clashing and entangling with each other in such limited space. Mitochondria form extensive networks constantly remodeled by fission and fusion. Here, we show that mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of mitochondria – via encounter with motile intracellular pathogens, via external pressure applied by an atomic force microscope, or via cell migration across uneven microsurfaces – results in the recruitment of the mitochondrial fission machinery, and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria, acts as a membrane-bound force sensor to recruit the fission machinery to mechanically strained sites. Thus, mitochondria adapt to the environment by sensing and responding to biomechanical cues. Our findings that mechanical triggers can be coupled to biochemical responses in membrane dynamics may explain how organelles orderly cohabit in the crowded cytoplasm.},
  author       = {Helle, Sebastian Carsten Johannes and Feng, Qian and Aebersold, Mathias J and Hirt, Luca and Grüter, Raphael R and Vahid, Afshin and Sirianni, Andrea and Mostowy, Serge and Snedeker, Jess G and Šarić, Anđela and Idema, Timon and Zambelli, Tomaso and Kornmann, Benoît},
  issn         = {2050-084X},
  journal      = {eLife},
  keywords     = {general immunology and microbiology, general biochemistry, genetics and molecular biology, general medicine, general neuroscience},
  publisher    = {eLife Sciences Publications},
  title        = {{Mechanical force induces mitochondrial fission}},
  doi          = {10.7554/elife.30292},
  volume       = {6},
  year         = {2017},
}