Characterization of Liguleless narrow, a dominant mutant controlling leaf development in Zea mays.

摘要

Maize leaves arise from the shoot apical meristem in a distichous pattern. Downregulation of knox genes in a subset of cells leads to the formation of a leaf primordia that develops into a phytomer which consists of a leaf, an internode, and an axillary bud. The maize leaf differentiates into distinct tissue types along the proximodistal axis; the distal blade, proximal sheath, and the blade-sheath boundary where ligule and auricle exist. The semi-dominant mutant Liguleless narrow (Lgn) was isolated as a half plant chimera in a B73 EMS mutagenized population. Lgn-R heterozygotes have narrower and shorter leaves with a defective ligular region. Auricles are missing and ligules occur over the midrib but fail to extend to the margins. This defect in ligule and auricle initiates early in leaf development when the blade-sheath boundary is established and preligular band forms. A continous preligular band is not observed in Lgn-R heterozygotes. Due to the defect in boundary establishment, the boundary epidermis consists of mixed cell identities and extension of proximal sheath tissue into the blade is observed. Lgn-R heterozygotes also display defects in reproductive development, such as reduced tassel branch, and failure to ear formation. These defects become more severe as a homozygote. The Lgn-R mutation has a subtle effect in the Mo17 background. Crossing the mutant to intermated B73 MoI7 (IBM) population revealed two regions on chromosome 1 that might contain the putative dominant suppressors in Mo17.;Double mutant analysis of Lgn-R with dominant Kn1 alleles revealed that the Lgn-R mutation does not affect the function of KN1 in establishing proximodistal axes but downregulates the activity of KN1 either transcriptionally or post-translationally. In order to understand the function of LGN in ligular region development, double mutants were generated with 1g1-R and 1g2-R. Results show that lgl-R is epistatic to Lgn-R while 1g2-R and Lgn-R act additively to control ligule and auricle development. The Lgn-R mutation eliminates the ectopic auricle phenotype of Wab1 and displays a very narrow leaf which is reminiscent of Wab1 lg1. This result, in addition to the lg double mutant results suggest that Lgn-R functions in the LG pathway. When Lgn-R is combined with ns, leaves become narrower and end in a blunted end. Since the Lgn-R blade has a normal tapered end, this indicates that the marginal domain specified by NS is unaffected in Lgn-R and the narrow leaf phenotype results from inhibition of growth in a different domain.;Positional cloning identified a Ser/Thr receptor like kinase to be a candidate lgn gene. The Lgn-R mutation results in decreased kinase activity suggesting that the mutation is dominant negative. A paralog of the LGN protein exists in maize and orthologs of the two proteins were found in other grasses. Phylogenetic analysis suggests that the duplication of LGN occurred before the speciation of the grasses.