A rho scaffold integrates the secretory system with feedback mechanisms in regulation of auxin distribution.
A rho scaffold integrates the secretory system with feedback mechanisms in regulation of auxin distribution.
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DOI:
10.1371/journal.pbio.1000282
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发表时间:
2010-01-19
期刊:
影响因子:
9.8
通讯作者:
Yalovsky S
中科院分区:
文献类型:
--
作者:
Hazak O;Bloch D;Poraty L;Sternberg H;Zhang J;Friml J;Yalovsky S
In plants, auxin distribution and tissue patterning are coordinated via a feedback loop involving the auxin-regulated cell polarity factor ICR1 and the secretory machinery. Development in multicellular organisms depends on the ability of individual cells to coordinate their behavior by means of small signaling molecules to form correctly patterned tissues. In plants, a unique mechanism of directional transport of the signaling molecule auxin between cells connects cell polarity and tissue patterning and thus is required for many aspects of plant development. Direction of auxin flow is determined by polar subcellular localization of PIN auxin efflux transporters. Dynamic PIN polar localization results from the constitutive endocytic cycling to and from the plasma membrane, but it is not well understood how this mechanism connects to regulators of cell polarity. The Rho family small GTPases ROPs/RACs are master regulators of cell polarity, however their role in regulating polar protein trafficking and polar auxin transport has not been established. Here, by analysis of mutants and transgenic plants, we show that the ROP interactor and polarity regulator scaffold protein ICR1 is required for recruitment of PIN proteins to the polar domains at the plasma membrane. icr1 mutant embryos and plants display an a array of severe developmental aberrations that are caused by compromised differential auxin distribution. ICR1 functions at the plasma membrane where it is required for exocytosis but does not recycle together with PINs. ICR1 expression is quickly induced by auxin but is suppressed at the positions of stable auxin maxima in the hypophysis and later in the embryonic and mature root meristems. Our results imply that ICR1 is part of an auxin regulated positive feedback loop realized by a unique integration of auxin-dependent transcriptional regulation into ROP-mediated modulation of cell polarity. Thus, ICR1 forms an auxin-modulated link between cell polarity, exocytosis, and auxin transport-dependent tissue patterning. The coordination of different cells during pattern formation is a fundamental process in the development of multicellular organisms. In plants, a unique mechanism of directional transport of the signaling molecule auxin between cells demonstrates the importance of cell polarity for tissue patterning. The direction of auxin flow is determined by polar subcellular localization of auxin transport proteins called PINs, which facilitate auxin efflux. At the same time, an auxin-mediated positive feedback mechanism reinforces the polar distribution of PINs. However, the molecular mechanisms that underlie polar PIN localization are not well understood. In eukaryotic cells, the Rho family of small GTPases function as central regulators of cell polarity. We show that a Rho-interacting protein from plants, called ICR1, is required for recruitment via the secretory system of PIN proteins to polar domains in the cell membrane. As a result, ICR1 is required for directional auxin transport and distribution and thereby for proper pattern formation. In addition, both the expression and subcellular localization of ICR1 are regulated by auxin, suggesting that ICR1 could function in a positive feedback loop that reinforces auxin distribution. Thus, ICR1 forms an auxin-modulated link between cell polarity, protein secretion, and auxin-dependent tissue patterning.
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影响因子:
3.3
作者:
Bloch, D;Lavy, M;Yalovsky, S
通讯作者:
Yalovsky, S
影响因子:
64.5
作者:
Geldner, N;Anders, N;Jürgens, G
通讯作者:
Jürgens, G
影响因子:
7.8
作者:
Kost, B;Lemichez, E;Spielhofer, P;Hong, Y;Tolias, K;Carpenter, C;Chua, N H
通讯作者:
Chua, N H
影响因子:
9.2
作者:
Eshed, Y;Baum, SF;Bowman, JL
通讯作者:
Bowman, JL
影响因子:
64.8
作者:
Dhonukshe, Pankaj;Tanaka, Hirokazu;Goh, Tatsuaki;Ebine, Kazuo;Mahonen, Ari Pekka;Prasad, Kalika;Blilou, Ikram;Geldner, Niko;Xu, Jian;Uemura, Tomohiro;Chory, Joanne;Ueda, Takashi;Nakano, Akihiko;Scheres, Ben;Friml, Jiri
通讯作者:
Friml, Jiri