Identifying genes that interact with Tp1 and Tp2

The phenotype of Tp1 and Tp2 suggests that these loci play an important role in regulating the transition from juvenile to adult growth in corn. In order to define loci that interact with Tp1 and Tp2 I have taken 2 different approaches. The first involves testing the effect of hyperploidy for various chromosome arms on the expression of these mutations. This approach is based on the assumption that the effect of such gross variation in chromosome dose can be traced to one or a few genes within the hyperploid region. Having defined chromosomal regions that interact with Tp1 and Tp2, the loci responsible for this effect can then be identified by efficient mutagenesis schemes. The second approach involves making "educated guesses" (based on the phenotypes of existing mutations) to search for mutations that interact synergistically with Tp1 and Tp2. Preliminary results indicate that both approaches have considerable merit.

Tp1/+ and Tp2/+ stocks homozygous for various recessive endosperm markers were crossed by appropriate B-A translocations in order to generate diploid, hypoploid and hyperploid progeny. Seeds with mutant endosperms were assumed to have hyperploid embryos. Those with wild type endosperms were assumed to be either diploid or hypoploid; the latter class should be relatively infrequent because of the low rate of B-A non-disjunction in a W23 background, and because B-A deficient sperm preferentially fertilize the central cell. Plants that were smaller than normal were assumed to be hypoploid escapes and were excluded from this analysis.

Of the arms that have been tested so far (1L, 3L, 4L, 5S, 5L, 6L, 9S, 10L), only 3 had obvious effects on the expression of Tp1 and/or Tp2. Hyperploidy for 1L suppresses tiller production by Tp1 plants, but enhances the effect of this mutation on tassel morphology. Hyperploidy for 3L and hyperploidy for 4L enhances the effects of Tp1 and Tp2 on both vegetative and reproductive morphology. Although other arms also had an effect on the morphology of Tp1 and Tp2, these effects were considered non-specific because wild type hyperploid siblings were similarly affected.

The fact that hyperploidy for 1L and 4L significantly influences the expression of Tp1 and Tp2 is particularly interesting because both arms possess mutations that interact synergistically with Tp1 and Tp2. Plants homozygous for teosinted branched (tb), a recessive mutation on 1L that enhances tillering and transforms the ear into a tassel, and heterozygous for Tp1 or Tp2 have dramatically more tillers than singly mutant plants; even tillers bear tillers in double mutants. The effect of this combination on reproductive development is unclear because in some families all primary branches terminate in a tassel, while in others, primary branches terminate in ears. However, as a rule, secondary branches are female.

It should be noted that the effect of tb on tiller formation in double mutants is the exact opposite of that produced by hyperploidy for 1L: i.e., increasing tb+ suppresses tillering while a recessive (presumably loss-of-function) mutation of this locus enhances tillering. This observation is consistent with the hypothesis that the Tp1 and Tp2 mutations enhance tiller formation (at least in part) by suppressing the expression of tb+. However, tb is clearly not the only locus involved in this process because grassy tillers (gt) also interacts synergistically with Tp1 and Tp2, although not to the same extent as tb.

The mutation of interest on 4L is Tu, a dominant mutation that increases glume size in heterozygous condition and has more extreme effects in homozygous condition. Since Tp1 and Tp2 also increase the size of glumes, and often transform them into leaf-like structures, it was of interest to determine how these loci interacted with Tu. Tu1+; Tp1/+ (or Tp2/+) plants have highly modified tassels and ears in which all vegetative structures are considerably larger than those produced by any of these mutations individually. One possible explanation for this result is that Tp1 and Tp2 stimulate the expression of Tu+, and Tu is a hypermorphic (over-expressing) mutation that enhances this stimulatory effect. A problem with this explanation is that dosage analysis of Tu indicates that this mutation is neomorphic rather than hypermorphic (MNL 61:85). If Tu is a constitutively active mutation, this explanation may have some validity.

R.S. Poethig


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