Abstract
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.