Agriculturally advantageous reduction in plant height is usually achieved by blocking the action or production of gibberellins. Here, we describe a different dwarfing mechanism found in maize brachytic2 (br2) mutants characterized by compact lower stalk internodes. The height reduction in these plants results from the loss of a P-glycoprotein that modulates polar auxin transport in the maize stalk. The sorghum ortholog of br2 is dwarf3 (dw3), an unstable mutant of long-standing commercial interest and concern. A direct duplication within the dw3 gene is responsible for its mutant nature and also for its instability, because it facilitates unequal crossing-over at the locus.
The HM1 gene in maize controls both race-specific resistance to the fungus Cochliobolus carbonum race 1 and expression of the NADPH (reduced form of nicotinamide adenine dinucleotide phosphate)-dependent HC toxin reductase (HCTR), which inactivates HC toxin, a cyclic tetrapeptide produced by the fungus to permit infection. Several HM1 alleles were generated and cloned by transposon-induced mutagenesis. The sequence of wild-type HM1 shares homology with dihydroflavonol-4-reductase genes from maize, petunia, and snap-dragon. Sequence homology is greatest in the beta alpha beta-dinucleotide binding fold that is conserved among NADPH- and NADH (reduced form of nicotinamide adenine dinucleotide)-dependent reductases and dehydrogenases. This indicates that HM1 encodes HCTR.
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