TY - JOUR A1 - Omidbakhshfard, Mohammad Amin A1 - Proost, Sebastian A1 - Fujikura, Ushio A1 - Müller-Röber, Bernd T1 - Growth-Regulating Factors (GRFs): A Small Transcription Factor Family with Important Functions in Plant Biology JF - Molecular plant N2 - Growth-regulating factors (GRFs) are plant-specific transcription factors that were originally identified for their roles in stem and leaf development, but recent studies highlight them to be similarly important for other central developmental processes including flower and seed formation, root development, and the coordination of growth processes under adverse environmental conditions. The expression of several GRFs is controlled by microRNA miR396, and the GRF-miRNA396 regulatory module appears to be central to several of these processes. In addition, transcription factors upstream of GRFs and miR396 have been discovered, and gradually downstream target genes of GRFs are being unraveled. Here, we review the current knowledge of the biological functions performed by GRFs and survey available molecular data to illustrate how they exert their roles at the cellular level. KW - abiotic stress KW - chromatin remodeling KW - flower development KW - growth regulation KW - leaf development KW - miRNA Y1 - 2015 U6 - https://doi.org/10.1016/j.molp.2015.01.013 SN - 1674-2052 SN - 1752-9867 VL - 8 IS - 7 SP - 998 EP - 1010 PB - Cell Press CY - Cambridge ER - TY - JOUR A1 - Omidbakhshfard, Mohammad Amin A1 - Fujikura, Ushio A1 - Olas, Justyna Jadwiga A1 - Xue, Gang-Ping A1 - Balazadeh, Salma A1 - Mueller-Roeber, Bernd T1 - GROWTH-REGULATING FACTOR 9 negatively regulates arabidopsis leaf growth by controlling ORG3 and restricting cell proliferation in leaf primordia JF - PLoS Genetics : a peer-reviewed, open-access journal N2 - 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. Y1 - 2018 U6 - https://doi.org/10.1371/journal.pgen.1007484 SN - 1553-7404 VL - 14 IS - 7 PB - PLoS CY - San Fransisco ER - TY - JOUR A1 - Katagiri, Yohei A1 - Hasegawa, Junko A1 - Fujikura, Ushio A1 - Hoshino, Rina A1 - Matsunaga, Sachihiro A1 - Tsukaya, Hirokazu T1 - The coordination of ploidy and cell size differs between cell layers in leaves JF - Development : Company of Biologists N2 - Growth and developmental processes are occasionally accompanied by multiple rounds of DNA replication, known as endoreduplication. Coordination between endoreduplication and cell size regulation often plays a crucial role in proper organogenesis and cell differentiation. Here, we report that the level of correlation between ploidy and cell volume is different in the outer and inner cell layers of leaves of Arabidopsis thaliana using a novel imaging technique. Although there is a well-known, strong correlation between ploidy and cell volume in pavement cells of the epidermis, this correlation was extremely weak in palisade mesophyll cells. Induction of epidermis cell identity based on the expression of the homeobox gene ATML1 in mesophyll cells enhanced the level of correlation between ploidy and cell volume to near that of wild-type epidermal cells. We therefore propose that the correlation between ploidy and cell volume is regulated by cell identity. KW - Endoreduplication KW - Ploidy KW - Cell volume KW - Mesophyll tissue KW - Epidermis KW - ATML1 Y1 - 2016 U6 - https://doi.org/10.1242/dev.130021 SN - 0950-1991 SN - 1477-9129 VL - 143 SP - 1120 EP - 1125 PB - Company of Biologists Limited CY - Cambridge ER - TY - JOUR A1 - Fujikura, Ushio A1 - Jing, Runchun A1 - Hanada, Atsushi A1 - Takebayashi, Yumiko A1 - Sakakibara, Hitoshi A1 - Yamaguchi, Shinjiro A1 - Kappel, Christian A1 - Lenhard, Michael T1 - Variation in splicing efficiency underlies morphological evolution in capsella JF - Developmental cell N2 - 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. Y1 - 2017 U6 - https://doi.org/10.1016/j.devcel.2017.11.022 SN - 1534-5807 SN - 1878-1551 VL - 44 IS - 2 SP - 192 EP - 203 PB - Cell Press CY - Cambridge ER - TY - JOUR A1 - Fujikura, Ushio A1 - Elsaesser, Lore A1 - Breuninger, Holger A1 - Sanchez-Rodriguez, Clara A1 - Ivakov, Alexander A1 - Laux, Thomas A1 - Findlay, Kim A1 - Persson, Staffan A1 - Lenhard, Michael T1 - Atkinesin-13A modulates cell-wall synthesis and cell expansion in arabidopsis thaliana via the THESEUS1 pathway JF - PLoS Genetics : a peer-reviewed, open-access journal N2 - 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. Y1 - 2014 U6 - https://doi.org/10.1371/journal.pgen.1004627 SN - 1553-7390 SN - 1553-7404 VL - 10 IS - 9 PB - PLoS CY - San Fransisco ER -