The Experts below are selected from a list of 38430 Experts worldwide ranked by ideXlab platform
Hiro-yuki Hirano - One of the best experts on this subject based on the ideXlab platform.
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Antagonistic action of TILLERS ABSENT1 and FLORAL ORGAN NUMBER2 regulates Stem Cell Maintenance during axillary meriStem development in rice.
The New phytologist, 2019Co-Authors: Wakana Tanaka, Hiro-yuki HiranoAbstract:Shoot branches are formed from the axillary meriStem and their formation is a key process in plant development. Although our understanding of the mechanisms underlying Stem Cell Maintenance in the shoot apical meriStem (SAM) is progressing, our knowledge of these mechanisms during the process of axillary meriStem development is insufficient. To elucidate the genetic mechanisms underlying axillary meriStem development in rice (Oryza sativa), we undertook a molecular genetic analysis focusing on TILLERS ABSENT1 (TAB1) and FLORAL ORGAN NUMBER2 (FON2), respective orthologs of the WUSCHEL and CLAVATA3 genes involved in SAM Maintenance in Arabidopsis (Arabidopsis thaliana). We revealed that Stem Cells were established at an early stage of axillary meriStem development in the wild-type, but were not maintained in tab1. By contrast, the Stem Cell region and TAB1 expression domain were expanded in fon2, and FON2 overexpression inhibited axillary meriStem formation. These results indicate that TAB1 is required to maintain Stem Cells during axillary meriStem development, whereas FON2 negatively regulates Stem Cell fate by restricting TAB1 expression. Thus, the genetic pathway regulating SAM Maintenance in Arabidopsis seems to have been recruited to play a specific role within a narrow developmental window - namely, axillary meriStem establishment - in rice.
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TILLERS ABSENT1, the WUSCHEL ortholog, is not involved in Stem Cell Maintenance in the shoot apical meriStem in rice.
Plant signaling & behavior, 2019Co-Authors: Chie Suzuki, Wakana Tanaka, Hiroyuki Tsuji, Hiro-yuki HiranoAbstract:Stem Cell Maintenance in the shoot apical meriStem (SAM) is very important for plant development and is regulated by the WUSCHEL-CLAVATA (WUS-CLV) feedback loop in Arabidopsis (Arabidopsis thaliana). WUS promotes Stem Cell identity, whereas CLV negatively regulates Stem Cell proliferation by repressing WUS expression. We previously showed that, in rice (Oryza sativa), the WUS ortholog TILLERS ABSENT1 (TAB1, also known as OsWUS) has no function in SAM Maintenance, whereas it plays a crucial role in axillary meriStem development. Recently, we showed that a double mutant of FLORAL ORGAN NUMBER2 (FON2) and ABERRANT SPIKELET AND PANICLE1 (ASP1) led to a marked enlargement of the inflorescence meriStem, and that the TAB1 function is not associated with massive Stem Cells in this meriStem. In this paper, we confirmed that TAB1 is also unrelated to the enlargement of the SAM in the vegetative phase of the fon2 and fon2 asp1 mutants. In addition, misexpression of TAB1 under the promoter of FON1 led to a slight reduction of the SAM size in wild type, suggesting that TAB1 is not a positive regulator of Stem Cells. Taking together, TAB1 seems not to be involved in meriStem Maintenance, irrespective of the meriStem type.
Zhenghui Quan - One of the best experts on this subject based on the ideXlab platform.
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tsc1 2 regulates intestinal Stem Cell Maintenance and lineage differentiation through rheb torc1 s6k but independently of nutritional status or notch regulation
Journal of Cell Science, 2013Co-Authors: Zhenghui Quan, Rongwen XiAbstract:Summary Tubular sclerosis complex gene products TSC1 and TSC2 have evolutionarily conserved roles in Cell growth from Drosophila to mammals. Here we reveal important roles for TSC1/2 in regulating intestinal Stem Cell (ISC) Maintenance and differentiation of the enteroendocrine Cell lineage in the Drosophila midgut. Loss of either the Tsc1 or Tsc2 gene in ISCs causes rapid ISC loss through TORC1 hyperactivation, because ISCs can be efficiently rescued by mutation of S6k or by rapamycin treatment. In addition, overexpression of Rheb, which triggers TORC1 activation, recapitulates the phenotype caused by TSC1/2 disruption. Genetic studies suggest that TSC1/2 maintains ISCs independently of nutritional status or Notch regulation, probably by inhibiting Cell delamination. We show that Tsc1/Tsc2 mutant ISCs can efficiently produce enterocytes but not enteroendocrine Cells, and this altered differentiation potential is also caused by hyperactivation of TORC1. Reduced TORC1–S6K signaling by mutation of S6k, however, has no effect on ISC Maintenance or Cell lineage differentiation. Our studies demonstrate that hyperactivation of TORC1 following the loss of TSC1/2 is detrimental to Stem Cell Maintenance and multiple lineage differentiation in the Drosophila ISC lineage, a mechanism that could be conserved in other Stem Cell lineages, including that in humans.
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TSC1/2 regulates intestinal Stem Cell Maintenance and lineage differentiation through Rheb-TORC1-S6K but independently of nutritional status or Notch regulation.
Journal of Cell Science, 2013Co-Authors: Zhenghui Quan, Pei Sun, Guonan LinAbstract:Tubular sclerosis complex gene products TSC1 and TSC2 have evolutionarily conserved roles in Cell growth from Drosophila to mammals. Here we reveal important roles for TSC1/2 in regulating intestinal Stem Cell (ISC) Maintenance and differentiation of the enteroendocrine Cell lineage in the Drosophila midgut. Loss of either the Tsc1 or Tsc2 gene in ISCs causes rapid ISC loss through TORC1 hyperactivation, because ISCs can be efficiently rescued by mutation of S6k or by rapamycin treatment. In addition, overexpression of Rheb, which triggers TORC1 activation, recapitulates the phenotype caused by TSC1/2 disruption. Genetic studies suggest that TSC1/2 maintains ISCs independently of nutritional status or Notch regulation, probably by inhibiting Cell delamination. We show that Tsc1/Tsc2 mutant ISCs can efficiently produce enterocytes but not enteroendocrine Cells, and this altered differentiation potential is also caused by hyperactivation of TORC1. Reduced TORC1-S6K signaling by mutation of S6k, however, has no effect on ISC Maintenance or Cell lineage differentiation. Our studies demonstrate that hyperactivation of TORC1 following the loss of TSC1/2 is detrimental to Stem Cell Maintenance and multiple lineage differentiation in the Drosophila ISC lineage, a mechanism that could be conserved in other Stem Cell lineages, including that in humans.
Henrik Jonsson - One of the best experts on this subject based on the ideXlab platform.
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plant Stem Cell Maintenance involves direct transcriptional repression of differentiation program
Molecular Systems Biology, 2013Co-Authors: Carolyn Ohno, Mariano Perales, Thomas Girke, Marcus G Heisler, Henrik Jonsson, Jérémy Gruel, Ram Kishor YadavAbstract:In animal syStems, master regulatory transcription factors (TFs) mediate Stem Cell Maintenance through a direct transcriptional repression of differentiation promoting TFs. Whether similar mechanisms operate in plants is not known. In plants, shoot apical meriStems serve as reservoirs of Stem Cells that provide Cells for all above ground organs. WUSCHEL, a homeodomain TF produced in Cells of the niche, migrates into adjacent Cells where it specifies Stem Cells. Through high-resolution genomic analysis, we show that WUSCHEL represses a large number of genes that are expressed in differentiating Cells including a group of differentiation promoting TFs involved in leaf development. We show that WUS directly binds to the regulatory regions of differentiation promoting TFs; KANADI1, KANADI2, ASYMMETRICLEAVES2 and YABBY3 to repress their expression. Predictions from a computational model, supported by live imaging, reveal that WUS-mediated repression prevents premature differentiation of Stem Cell progenitors, being part of a minimal regulatory network for meriStem Maintenance. Our work shows that direct transcriptional repression of differentiation promoting TFs is an evolutionarily conserved logic for Stem Cell regulation.
Guonan Lin - One of the best experts on this subject based on the ideXlab platform.
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TSC1/2 regulates intestinal Stem Cell Maintenance and lineage differentiation through Rheb-TORC1-S6K but independently of nutritional status or Notch regulation.
Journal of Cell Science, 2013Co-Authors: Zhenghui Quan, Pei Sun, Guonan LinAbstract:Tubular sclerosis complex gene products TSC1 and TSC2 have evolutionarily conserved roles in Cell growth from Drosophila to mammals. Here we reveal important roles for TSC1/2 in regulating intestinal Stem Cell (ISC) Maintenance and differentiation of the enteroendocrine Cell lineage in the Drosophila midgut. Loss of either the Tsc1 or Tsc2 gene in ISCs causes rapid ISC loss through TORC1 hyperactivation, because ISCs can be efficiently rescued by mutation of S6k or by rapamycin treatment. In addition, overexpression of Rheb, which triggers TORC1 activation, recapitulates the phenotype caused by TSC1/2 disruption. Genetic studies suggest that TSC1/2 maintains ISCs independently of nutritional status or Notch regulation, probably by inhibiting Cell delamination. We show that Tsc1/Tsc2 mutant ISCs can efficiently produce enterocytes but not enteroendocrine Cells, and this altered differentiation potential is also caused by hyperactivation of TORC1. Reduced TORC1-S6K signaling by mutation of S6k, however, has no effect on ISC Maintenance or Cell lineage differentiation. Our studies demonstrate that hyperactivation of TORC1 following the loss of TSC1/2 is detrimental to Stem Cell Maintenance and multiple lineage differentiation in the Drosophila ISC lineage, a mechanism that could be conserved in other Stem Cell lineages, including that in humans.
Rongwen Xi - One of the best experts on this subject based on the ideXlab platform.
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tsc1 2 regulates intestinal Stem Cell Maintenance and lineage differentiation through rheb torc1 s6k but independently of nutritional status or notch regulation
Journal of Cell Science, 2013Co-Authors: Zhenghui Quan, Rongwen XiAbstract:Summary Tubular sclerosis complex gene products TSC1 and TSC2 have evolutionarily conserved roles in Cell growth from Drosophila to mammals. Here we reveal important roles for TSC1/2 in regulating intestinal Stem Cell (ISC) Maintenance and differentiation of the enteroendocrine Cell lineage in the Drosophila midgut. Loss of either the Tsc1 or Tsc2 gene in ISCs causes rapid ISC loss through TORC1 hyperactivation, because ISCs can be efficiently rescued by mutation of S6k or by rapamycin treatment. In addition, overexpression of Rheb, which triggers TORC1 activation, recapitulates the phenotype caused by TSC1/2 disruption. Genetic studies suggest that TSC1/2 maintains ISCs independently of nutritional status or Notch regulation, probably by inhibiting Cell delamination. We show that Tsc1/Tsc2 mutant ISCs can efficiently produce enterocytes but not enteroendocrine Cells, and this altered differentiation potential is also caused by hyperactivation of TORC1. Reduced TORC1–S6K signaling by mutation of S6k, however, has no effect on ISC Maintenance or Cell lineage differentiation. Our studies demonstrate that hyperactivation of TORC1 following the loss of TSC1/2 is detrimental to Stem Cell Maintenance and multiple lineage differentiation in the Drosophila ISC lineage, a mechanism that could be conserved in other Stem Cell lineages, including that in humans.