The genetical basis of the Glu1 null phenotype is complex. GLU1 activity has been identified in hybrid Glu1 null x Glu1 plus seedlings. In some cases the appearance of two homodimers and the corresponding heterodimer has been reported (Goodman and Stuber, in Isozymes in Plant Genetics and Breeding, part B: 1, 1983; Rifaat and Esen, MNL 63:39, 1989). To explain these results Rifaat and Esen have proposed that the null phenotype is due to mutation of a trans-acting regulatory element and that partial complementation occurs in the null x plus hybrids. The picture, however, seems to be more complex than that.
I have analyzed the ß-GLU zymograms produced by different seedling tissues (coleoptiles, mesocotyls, scutellar node and roots) of lines H95 (Null), ND474 (Slow), N152 (Fast), H99 and L289 (Intermediate) and their F1s. The accompanying Figure shows that: A) the null phenotype is present only in coleoptilar tissue of H95, while mesocotyls, roots and, to a less extent, scutellar node possess a clear ß-GLU activity, which identifies the line as ß-Glu SS; and: B) with the exception of H95 x N152, in all other hybrids the coleoptile presents a null phenotype. In all cases mesocotyls show the expected 1 (H95 x ß-Glu SS) or 3 (H95 x ß-Glu FF) band pattern.
The results suggest that the null phenotype in line H95 is: 1) tissue specific; and 2) that a trans acting regulatory element is indeed involved in its determination, but it appears to be a repressor rather than an activator, and behaves as dominant in null x plus F s. The reasons why in hybrid H95 x N152 coleoptiles ß-GLU activity, although weaker than normal, is expressed are at present unclear.
The data also show an additional, more anodal band in the roots of Glu1 SS genotypes. Its absence in all Glu1 FF inbreds analyzed (not shown) could be due to electrophoretic overlapping with the GLU1 FF homodimer, but further analyses are required to clarify this point.
Several questions remain unanswered,
among which are: is the tissue specificity of the null phenotype peculiar
to one inbred line (H95) or common to other Glu1 nulls? Is the regulatory
element linked to the Glu1 locus and what is its precise mechanism
of action? Is the additional ß-GLU found in roots the product of
a different gene? All these points are currently under investigation.
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