@article{GrafDolzblaszWuerschumetal.2010,
  author    = {Graf, Philipp and Dolzblasz, Alicja and W{\"u}rschum, Tobias and Lenhard, Michael and Pfreundt, Ulrike and Laux, Thomas},
  title     = {MGOUN1 encodes an Arabidopsis type Ib DNA topoisomerase required in stem cell regulation and to maintain develpmentally regulated gene silencing},
  issn      = {1040-4651},
  year      = {2010},
  language  = {en}
}
@article{ViTrostLangeetal.2013,
  author    = {Vi, Son Lang and Trost, Gerda and Lange, Peggy and Czesnick, Hj{\"o}rdis and Rao, Nishta and Lieber, Diana and Laux, Thomas and Gray, William M. and Manley, James L. and Groth, Detlef and Kappel, Christian and Lenhard, Michael},
  title     = {Target specificity among canonical nuclear poly(A) polymerases in plants modulates organ growth and pathogen response},
  series = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
  volume    = {110},
  journal   = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA},
  number    = {34},
  publisher = {NATL ACAD SCIENCES},
  address   = {WASHINGTON},
  issn      = {0027-8424},
  doi       = {10.1073/pnas.1303967110},
  pages     = {13994 -- 13999},
  year      = {2013},
  abstract  = {Polyadenylation of pre-mRNAs is critical for efficient nuclear export, stability, and translation of the mature mRNAs, and thus for gene expression. The bulk of pre-mRNAs are processed by canonical nuclear poly(A) polymerase (PAPS). Both vertebrate and higher-plant genomes encode more than one isoform of this enzyme, and these are coexpressed in different tissues. However, in neither case is it known whether the isoforms fulfill different functions or polyadenylate distinct subsets of pre-mRNAs. Here we show that the three canonical nuclear PAPS isoforms in Arabidopsis are functionally specialized owing to their evolutionarily divergent C-terminal domains. A strong loss-of-function mutation in PAPS1 causes a male gametophytic defect, whereas a weak allele leads to reduced leaf growth that results in part from a constitutive pathogen response. By contrast, plants lacking both PAPS2 and PAPS4 function are viable with wild-type leaf growth. Polyadenylation of SMALL AUXIN UP RNA (SAUR) mRNAs depends specifically on PAPS1 function. The resulting reduction in SAUR activity in paps1 mutants contributes to their reduced leaf growth, providing a causal link between polyadenylation of specific pre-mRNAs by a particular PAPS isoform and plant growth. This suggests the existence of an additional layer of regulation in plant and possibly vertebrate gene expression, whereby the relative activities of canonical nuclear PAPS isoforms control de novo synthesized poly(A) tail length and hence expression of specific subsets of mRNAs.},
  language  = {en}
}
@article{FujikuraElsaesserBreuningeretal.2014,
  author    = {Fujikura, Ushio and Elsaesser, Lore and Breuninger, Holger and Sanchez-Rodriguez, Clara and Ivakov, Alexander and Laux, Thomas and Findlay, Kim and Persson, Staffan and Lenhard, Michael},
  title     = {Atkinesin-13A modulates cell-wall synthesis and cell expansion in arabidopsis thaliana via the THESEUS1 pathway},
  series = {PLoS Genetics : a peer-reviewed, open-access journal},
  volume    = {10},
  journal   = {PLoS Genetics : a peer-reviewed, open-access journal},
  number    = {9},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1553-7390},
  doi       = {10.1371/journal.pgen.1004627},
  pages     = {15},
  year      = {2014},
  abstract  = {Growth of plant organs relies on cell proliferation and expansion. While an increasingly detailed picture about the control of cell proliferation is emerging, our knowledge about the control of cell expansion remains more limited. We demonstrate the internal-motor kinesin AtKINESIN-13A (AtKIN13A) limits cell expansion and cell size in Arabidopsis thaliana, ion atkinl3a mutants forming larger petals with larger cells. The homolog, AtKINESIN-13B, also affects cell expansion and double mutants display growth, gametophytic and early embryonic defects, indicating a redundant role of he two genes. AtKIN13A is known to depolymerize microtubules and influence Golgi motility and distribution. Consistent his function, AtKIN13A interacts genetically with ANGUSTIFOLIA, encoding a regulator of Golgi dynamics. Reduced AtIGN13A activity alters cell wall structure as assessed by Fourier-transformed infrared-spectroscopy and triggers signalling he THESEUS1-dependent cell-wall integrity pathway, which in turn promotes the excess cell expansion in the atkinl3a mutant. Thus, our results indicate that the intracellular activity of AtKIN13A regulates cell expansion and wall architecture via THESEUS1, providing a compelling case of interplay between cell wall integrity sensing and expansion.},
  language  = {en}
}