Article Addendum

TOR pathway activation in Zea mays L. tissues: Conserved function between animal and plant kingdoms

Volume 7, Issue 6   June 2012
Pages 675 - 677
http://dx.doi.org/10.4161/psb.19993
Keywords: TOR pathway, ZmIGF maize growth factor, cell growth and proliferation, ribosome biogenesis, translational control
Authors: Verónica Garrocho-Villegas and Estela Sánchez de Jiménez

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Abstract:
In most non-photosynthetic eukaryotes it has been demonstrated a conserved signal transduction pathway, namely TOR-S6K, that coordinates growth and cell proliferation. This pathway targets the translational apparatus to induce selective translation of ribosomal mRNAs as well as stimulate the cell cycle transition through the G1/S phase. Thus, by activation of this pathway through environmental signals, nutrients, stress, or specific growth factors, such as insulin or insulin-like growth factors (IGF), this pathway allows organisms to regulate growth and cell division. In plants, evidence has shown that TOR protein has been highly conserved through evolution, being involved in growth and cell proliferation control as well. Particularly in maize, a peptide named ZmIGF has been found in actively growing tissues. It targets the maize TOR pathway at the same extent as insulin and, by doing so it induces growth, as well as ribosomal proteins and DNA synthesis. Thus, higher metazoans and plants seem to conserve similar biochemical paths to regulate cell growth through equivalent targets that conduce to activation of the TOR-S6K pathway. Recent research shows evidence that supports this proposal by uncovering the ZmIGF receptor in maize, providing further means for analyzing the role of the conserved TOR signaling pathway in this plant.

Article Addendum to:
R Sotelo, V Garrocho-Villegas, CR Aguilar, ME Calderon, de Jimenez E Sanchez. Coordination of cell growth and cell division in maize (Zea mays L.) relevance of the conserved TOR signal transduction pathway. In Vitro Cell Dev Biol-Plant 2010; 46: 578-86
DOI: 10.1007/s11627-010-9293-8

Received: March 9, 2012; Accepted: March 12, 2012; Published Online: May 14, 2012

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