The identification of L1-expressed genes, and the subsequent characterisation of their promoters, coupled to the identification of key growth regulators in plants, has recently smoothed the way for a new generation of experiments aimed at understanding the contribution of the L1 to plant growth. Two independent studies have used expression of cognate growth regulators under the ATML1 promoter to analyse how manipulating growth specifically in the L1 of the SAM and young leaf primordia affects organ development.
In the first study two cyclin-dependent kinase inhibitors, KRP1/ICK1 and KRP4, were expressed in the L1, leading to a decrease in L1 proliferation. The resulting epidermal cells demonstrated a compensatory increase in size, but overall plant and organ size were none-the-less decreased. Surprisingly however, cell numbers in the underlying mesophyll did not differ significantly from those in wild-type leaves leading the authors to conclude that the control of proliferation in mesophyll and epidermal cell layers are regulated by autonomous programmes during development (Bemis and Torii 2007). This conclusion is in agreement with those reached during the study of the reticulata mutant (Sect. 3.6) (Gonzalez-Bayon et al. 2006). However, during wild-type development, cessation of cell division in the epidermis occurs later than that in underlying tissues (Sect. 3.3). Moreover, no effect on the SAM was observed in this study, suggesting that the transgenic KRP activity may be context dependent. It is thus possible that the KRP-induced block in cell division in this study could function predominantly at stages in primordium development when mesophyll proliferation is more advanced than that of the epidermis, leading, in part, to the observed imbalance in cell-numbers in the mature leaves.
The second study used a similar strategy to reintroduce perception of the growth-promoting molecule brassinosteroid (br) specifically in the L1 layer of dwarf brassinosteroid insensitive mutants. This was sufficient to rescue normal organ growth, despite the fact that br perception appeared to occur largely cell autonomously. Moreover, depletion of br in the L1 was sufficient to cause dwarfing. It was concluded, in line with several clonal studies discussed previously, that a non-cell-autonomous signal from the epidermis controls the growth of underlying cells allowing the epidermis to both drive and restrict the growth of shoots (Savaldi-Goldstein et al. 2007).
When considering the apparently contradictory conclusions drawn from these studies, it should be borne in mind that the control of growth mediated by br acts predominantly (although not exclusively) at the level of cell expansion, whereas KRPs exert a direct control of cell proliferation. This not only serves to make the two sets of observations difficult to compare directly, but also underlines the potential complexity, as well as the utility, of analysing growth control using such approaches.
Was this article helpful?