A new mutant allele of Brachytic 2 maize gene

Plants with short stature have had a big impact on agriculture. World rice and wheat grain yields increased dramatically in the l960s and 1970s (green revolution) because farmers adopted new varieties that were shorter and more resistant to storm damage. Brachytic/dwarf varieties have not been exploited commercially in maize, partly because of the excessively severe nature of the original mutant alleles. However similar mutations have been used extensively in sorghum production since the 1950s. To our knowledge, there are three brachytic mutants isolated so far in maize: brachytic1 (br1), brachytic2 (br2) and brachytic3 (br3) that show a short stature and gibberellin insensitive phenotype A maize brachytic mutant of agronomic potential is the recessive br2 mutation, which results in the shortening of lower stalk internodes. br2 was cloned by transposon tagging with Mu element by Multani et al., in 2003 and it encodes a putative protein similar to adenosine triphosphate (ATP)- binding cassette transporters of the multidrug resistant (MDR) class of P-glycoproteins (PGPs) involved in polar movement of auxins. The spontaneous maize mutant, named brachytic-23* (br*-23), described in this work has a short stature and compact lower stalk internodes compared to wild type control. The genetic analysis indicated that br*-23 was inherited as a monogenic recessive trait. In allelism tests our mutant failed to complement the br2 mutant, thus it became obvious that br*-23 represents a mutation in the br2 gene. Following the guidelines provided by the Maize- GDB, we renamed the new mutation br2-23. In order to investigate the molecular lesion in the br2-23 allele, we designed specific primers on the basis of the sequence of the br2 gene cloned by transposon tagging by Multani et. al., in 2003. The genomic PCR fragments obtained from a homozygous mutant and a wild type plant (B73 inbred line) were subcloned and sequence analyses were performed. Preliminary alignment of Br2 (B73 Allele) and br2-23 sequences, performed using the CLUSTALW program, revealed that the mutant carries a eight nucleotide deletion in the coding region. The presence of this deletion in the coding region was also confirmed by using allele-specific primers. Details of further genetic, molecular, and histological characterization of this mutant will be presented.