RESUMEN
The parasitic weed Striga (Striga hermonthica) limits productivity of sorghum (Sorghum bicolor) and other cereals in sub-Saharan Africa and elsewhere. Improved host plant genetics is an effective control method but verified loci contributing to Striga resistance are limited. LOW GERMINATION STIMULANT 1 remains the only known sorghum locus affecting resistance to Striga. Functional loss (lgs1) alleles at this locus result in low Striga germination stimulant activity. We developed a robust polymerase chain reaction (PCR)-based LGS1 marker that detects all known natural lgs1 alleles. We have successfully used this marker to improve Striga resistance in our sorghum breeding program. To check its utility among diverse sets of germplasm, we genotyped 406 lines of the sorghum association panel (SAP) with the marker and phenotyped them for Striga germination stimulant activity. The SAP contains 23 lines (6%) with lgs1 mutations that involve a complete loss of this gene. Three previously described deletion alleles (lgs1-1, lgs1-2, and lgs1-3) ranging from 28.5 to 34 kbp are present among SAP members with a new one, lgs1-6, missing nearly 50 kbp relative to the reference genome. All 23 members of the SAP carrying lgs1 alleles had low Striga germination stimulant activity. The smaller previously described intragenic deletion mutations lgs1-4 and lgs1-5 are not present in the SAP. The LGS1 marker is useful for both detecting sources of lgs1 and introgressing Striga resistance into new genetic backgrounds.
RESUMEN
Genetic analysis of brown midrib sorghum (Sorghum bicolor) mutant lines assembled in our program has previously shown that the mutations fall into four allelic groups, bmr2, bmr6, bmr12 or bmr19. Causal genes for allelic groups bmr2, bmr6 and bmr12, have since been identified. In this report, we provide evidence for the nature of the bmr19 mutation. This was accomplished by introgressing each of the four bmr alleles into nine different genetic backgrounds. Polymorphisms from four resequenced bulks of sorghum introgression lines containing either mutation, relative to those of a resequenced bulk of the nine normal midrib recurrent parent lines, were used to locate their respective causal mutations. The analysis confirmed the previously reported causal mutations for bmr2 and bmr6 but failed in the case of bmr12-bulk due to a mixture of mutant alleles at the locus among members of that mutant bulk. In the bmr19-bulk, a common G â A mutation was found among all members in Sobic.001G535500. This gene encodes a putative folylpolyglutamate synthase with high homology to maize Bm4. The brown midrib phenotype co-segregated with this point mutation in two separate F2 populations. Furthermore, an additional variant allele at this locus obtained from a TILLING population also showed a brown midrib phenotype, confirming this locus as Bmr19.
