L1 Division and Differentiation Patterns Influence Shoot Apical Meristem Maintenance

Abstract

Plant development requires regulation of both cell division and differentiation. The class 1 KNOTTED1-like homeobox (KNOX) genes such as knotted1 (kn1) in maize (Zea mays) and SHOOTMERISTEMLESS in Arabidopsis (Arabidopsis thaliana) play a role in maintaining shoot apical meristem indeterminacy, and their misexpression is sufficient to induce cell division and meristem formation. KNOX overexpression experiments have shown that these genes interact with the cytokinin, auxin, and gibberellin pathways. The L1 layer has been shown to be necessary for the maintenance of indeterminacy in the underlying meristem layers. This work explores the possibility that the L1 affects meristem function by disrupting hormone transport pathways. The semidominant Extra cell layers1 (Xcl1) mutation in maize leads to the production of multiple epidermal layers by overproduction of a normal gene product. Meristem size is reduced in mutant plants and more cells are incorporated into the incipient leaf primordium. Thus, Xcl1 may provide a link between L1 division patterns, hormonal pathways, and meristem maintenance. We used double mutants between Xcl1 and dominant KNOX mutants and showed that Xcl1 suppresses the Kn1 phenotype but has a synergistic interaction with gnarley1 and rough sheath1, possibly correlated with changes in gibberellin and auxin signaling. In addition, double mutants between Xcl1 and crinkly4 had defects in shoot meristem maintenance. Thus, proper L1 development is essential for meristem function, and XCL1 may act to coordinate hormonal effects with KNOX gene function at the shoot apex.

The Maize Transcription Factor KNOTTED1 Directly Regulates the Gibberellin Catabolism Genega2ox1

“…Similar observations were made when crossing Kn1-N to the dominant Dwarf9 mutant (see Supplemental Figure 1 online). This finding is consistent with the increased knot formation observed after treatment of seedlings with a GA synthesis inhibitor (Kessler et al, 2006). In addition to the effect on plant height, the low GA level in d3 plants generates wider and shorter leaves (Table 1).…”

“…The genetic evidence described above indicates that KN1 is involved in GA metabolism, while at the molecular level, a previous study showed that the ga2ox1 mRNA level is increased in leaves of Kn1-N (Kessler et al, 2006). Since this gene encodes a GA catabolism enzyme, we hypothesized that it could represent one of the mechanistic links between KN1 and GA homeostasis.…”

“…Dwarfism is generally associated with a defect in GA synthesis, perception, or metabolism (Thomas et al, 2005), and dominant Kn1 mutants, such as Kn1-N, are shorter than their normal siblings. When Kn1-N mutants were supplemented with GA, the severity of the knotted phenotype (number of knots on leaves) was reduced, while it was aggravated when treating plants with an inhibitor of GA synthesis (Kessler et al, 2006). Accumulation of ga2ox1 mRNA, which encodes an enzyme involved in inactivation of bioactive GA, is elevated in leaves of the dominant mutant Kn1-N (Kessler et al, 2006).…”

“…When Kn1-N mutants were supplemented with GA, the severity of the knotted phenotype (number of knots on leaves) was reduced, while it was aggravated when treating plants with an inhibitor of GA synthesis (Kessler et al, 2006). Accumulation of ga2ox1 mRNA, which encodes an enzyme involved in inactivation of bioactive GA, is elevated in leaves of the dominant mutant Kn1-N (Kessler et al, 2006). GA2ox2 mRNA level is similarly increased in Arabidopsis leaves overexpressing STM, but because GA2ox2 mRNA is also upregulated in response to higher cytokinin levels, it remained unclear if the modulation was the indirect consequence of STM-induced cytokinin production (Jasinski et al, 2005).…”

Growth coordination and the shoot epidermis

“…At the same time it will be important to develop other molecular strategies, for example, to develop sensors that monitor the activity of a given hormone signaling pathway in real time. Finally, mutants which are specifically impaired in cell proliferation in the L1 can be used to further address its role in inter-cell-layer communication [39].…”