Lxm1-O suppresses the Kn1-O lateral vein phenotype

--Michael Freeling

Among the mutants that alter leaf development, a class of at least six genes, each defined by dominant mutant alleles, moves the position of the blade-sheath boundary in the leaf. This boundary is marked by the presence of the auricle and ligule. Mutants Kn1, Rs1, Lg3, Lg4, Hsf1 and Lxm1 all move the boundary out toward the tip of the blade, leading to the transformation of blade tissue to sheath tissue. No mutants have been observed that show the opposite polarity. Since Kn1's coding sequence contains a homeodomain (Hake in Wessler and Hake, 1990, The Plant Cell 2:495), fundamental regulatory levels are probably involved.

A Kn1-O homozygote in a background conditioning severe knotting and ectopic ligule formation around lateral veins was crossed to a Lxm1-O heterozygote. Lxm1-O is much like knotted, but it affects the midvein rather than the laterals, either because it only acts in very early plastochrons, or because it is midvein specific; its phenotype is retarded development around the midvein resulting in the sheath extending all the way to the tip of the leaf over the midvein. The progeny of this cross were all Kn1-O heterozygotes, but half were Lxm1-O double mutants and half were knotted only. Of the 15 plants examined, 7 were normally knotted and 8 appeared to be lax midvein only, with the knotted phenotype suppressed (Family 10960 plant 1 and plant 14 exemplify these two phenotypes in Fig. 1).

Figure 1.

There are two general ways this suppression could occur. Possibly, Lxm1 is an upstream regulator of Kn1 expression such that Lxm1 "turns off" Kn1 ectopic expression around lateral veins. A more biological and much more fun explanation is possible. Both Kn1 and Lxm1 mutants may be described as retarded (heterochronic) mutants in that the proper stage transitions from more juvenile to more adult move too slowly. Kn1 retards the developmental "schedule" around lateral veins (Freeling and Hake, 1985, Genetics 111:617) at about plastochron 4 while Lxm1 retards the developmental schedule for development controlled by the midvein. The suppression of Kn1 phenotype by Lxm1 is explained if the maturation of the midvein induces the laterals to begin their developmentally important inductive events. In this way, Kn1 mutants normally encode cells in lateral veins that are "too young for their ages," and--when they receive signals from the midvein that say "stop dividing" or "switch to blade identity" they continue on as if deaf (incompetence). However, if the midvein is also developmentally retarded, leaf development returns to synchrony. Just an idea.

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