Growth-limiting proteins in maize coleoptiles and the auxin-brassinosteroid hypothesis of mesocotyl elongation.

The shoot of grass coleoptiles consists of the mesocotyl, the node, and the coleoptile (with enclosed primary leaf). Since the 1930s, it is known that auxin (indole-3-acetic acid, IAA), produced in the tip of the coleoptile, is the central regulator of turgor-driven organ growth. Fifty years ago, it was discovered that antibiotics that suppress protein biosynthesis, such as cycloheximide, inhibit auxin (IAA)-induced cell elongation in excised sections of coleoptiles and stems. Based on such inhibitor studies, the concept of "growth-limiting proteins (GLPs)" emerged that was subsequently elaborated and modified. Here, we summarize the history of this idea with reference to IAA-mediated shoot elongation in maize (Zea mays) seedlings and recent studies on the molecular mechanism underlying auxin action in Arabidopsis thaliana. In addition, the analysis of light-induced inhibition of shoot elongation in intact corn seedlings is discussed. We propose a concept to account for the GLP-mediated epidermal wall-loosening process in coleoptile segments and present a more general model of growth regulation in intact maize seedlings. Quantitative proteomic and genomic studies led to a refinement of the classic "GLP concept" to explain phytohormone-mediated cell elongation at the molecular level (i.e., the recently proposed theory of a "central growth regulation network," CGRN). Novel data show that mesocotyl elongation not only depends on auxin but also on brassinosteroids (BRs). However, the biochemical key processes that regulate the IAA/BR-mediated loosening of the expansion-limiting epidermal wall(s) have not yet been elucidated.