Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.celrep.2018.04.033
Title: FTIP-Dependent STM Trafficking Regulates Shoot Meristem Development in Arabidopsis
Authors: Liu, L.
Li, C. 
Song, S. 
Teo, Z.W.N. 
Shen, L.
Wang, Y. 
Jackson, D.
Yu, H. 
Keywords: Arabidopsis
MCTP
organogenesis
protein trafficking
shoot meristem
stem cell
Issue Date: 2018
Publisher: Elsevier B.V.
Citation: Liu, L., Li, C., Song, S., Teo, Z.W.N., Shen, L., Wang, Y., Jackson, D., Yu, H. (2018). FTIP-Dependent STM Trafficking Regulates Shoot Meristem Development in Arabidopsis. Cell Reports 23 (6) : 1879-1890. ScholarBank@NUS Repository. https://doi.org/10.1016/j.celrep.2018.04.033
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
Abstract: Organogenesis in higher plants occurs in the shoot meristem, which contains pluripotent stem cells. Here, we show that two multiple C2 domain and transmembrane region proteins, FT INTERACTING PROTEIN 3 (FTIP3) and FTIP4, play an essential role in mediating proliferation and differentiation of shoot stem cells in Arabidopsis. FTIP3/4 prevent intracellular trafficking of a key regulator, SHOOTMERISTEMLESS (STM), to the plasma membrane in cells in the peripheral shoot meristem region. This facilitates STM recycling to the nucleus to maintain stem cells. Without FTIP3/4, STM localizes substantially to the plasma membrane, which promotes intercellular trafficking but compromises nuclear localization of STM. This accelerates stem cell differentiation, causing early termination of shoot apices and resulting in dwarf and bushy phenotypes. Our findings reveal a molecular framework that determines the fate of shoot stem cells and the resulting aboveground plant body. Liu et al. report that FTIP3 and FTIP4 control subcellular localization and intercellular trafficking of another key meristem regulator in the shoot apex. This determines the appropriate balance between the maintenance of shoot stem cells and their differentiation into other aboveground plant parts. © 2018 The Author(s)
Source Title: Cell Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/206449
ISSN: 2211-1247
DOI: 10.1016/j.celrep.2018.04.033
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
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