@article{OmidbakhshfardFujikuraOlasetal.2018,
  author    = {Omidbakhshfard, Mohammad Amin and Fujikura, Ushio and Olas, Justyna Jadwiga and Xue, Gang-Ping and Balazadeh, Salma and Mueller-Roeber, Bernd},
  title     = {GROWTH-REGULATING FACTOR 9 negatively regulates arabidopsis leaf growth by controlling ORG3 and restricting cell proliferation in leaf primordia},
  series = {PLoS Genetics : a peer-reviewed, open-access journal},
  volume    = {14},
  journal   = {PLoS Genetics : a peer-reviewed, open-access journal},
  number    = {7},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1553-7404},
  doi       = {10.1371/journal.pgen.1007484},
  pages     = {31},
  year      = {2018},
  abstract  = {Leaf growth is a complex process that involves the action of diverse transcription factors (TFs) and their downstream gene regulatory networks. In this study, we focus on the functional characterization of the Arabidopsis thaliana TF GROWTH-REGULATING FACTOR9 (GRF9) and demonstrate that it exerts its negative effect on leaf growth by activating expression of the bZIP TF OBP3-RESPONSIVE GENE 3 (ORG3). While grf9 knockout mutants produce bigger incipient leaf primordia at the shoot apex, rosette leaves and petals than the wild type, the sizes of those organs are reduced in plants overexpressing GRF9 (GRF9ox). Cell measurements demonstrate that changes in leaf size result from alterations in cell numbers rather than cell sizes. Kinematic analysis and 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay revealed that GRF9 restricts cell proliferation in the early developing leaf. Performing in vitro binding site selection, we identified the 6-base motif 5'-CTGACA-3' as the core binding site of GRF9. By global transcriptome profiling, electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) we identified ORG3 as a direct downstream, and positively regulated target of GRF9. Genetic analysis of grf9 org3 and GRF9ox org3 double mutants reveals that both transcription factors act in a regulatory cascade to control the final leaf dimensions by restricting cell number in the developing leaf.},
  language  = {en}
}
@article{FujikuraJingHanadaetal.2018,
  author    = {Fujikura, Ushio and Jing, Runchun and Hanada, Atsushi and Takebayashi, Yumiko and Sakakibara, Hitoshi and Yamaguchi, Shinjiro and Kappel, Christian and Lenhard, Michael},
  title     = {Variation in splicing efficiency underlies morphological evolution in capsella},
  series = {Developmental cell},
  volume    = {44},
  journal   = {Developmental cell},
  number    = {2},
  publisher = {Cell Press},
  address   = {Cambridge},
  issn      = {1534-5807},
  doi       = {10.1016/j.devcel.2017.11.022},
  pages     = {192 -- 203},
  year      = {2018},
  abstract  = {Understanding the molecular basis of morphological change remains a central challenge in evolutionary-developmental biology. The transition from outbreeding to selfing is often associated with a dramatic reduction in reproductive structures and functions, such as the loss of attractive pheromones in hermaphroditic Caenorhabditis elegans and a reduced flower size in plants. Here, we demonstrate that variation in the level of the brassinosteroid-biosynthesis enzyme CYP724A1 contributes to the reduced flower size of selfing Capsella rubella compared with its outbreeding ancestor Capsella grandiflora. The primary transcript of the C. rubella allele is spliced more efficiently than that of C. grandiflora, resulting in higher brassinosteroid levels. These restrict organ growth by limiting cell proliferation. More efficient splicing of the C. rubella allele results from two de novo mutations in the selfing lineage. Thus, our results highlight the potentially widespread importance of differential splicing efficiency and higher-than-optimal hormone levels in generating phenotypic variation.},
  language  = {en}
}