Marker assisted genetic analysis of non‐brittle rachis trait in barley

摘要

INTRODUCTIONHead shattering is a weedy character that causes serious yield losses in barley. Weak rachis and brittle rachis are two mechanisms of head shattering. For both mechanisms, shattering is dominant. In weak rachis, one or two breaks occur in the spikes. A major QTL for weak rachis, Hst-3, was mapped on the short arm of Chromosome 3 using molecular markers (Kandemir et al. 2000). Brittle rachis, on the other hand, causes multiple segmentations on a spike. In extreme brittleness, spikelets disarticulate easily and only a few spikelets remain on the spike. The non-brittle rachis trait is controlled by multiple genes. Some loci for non-brittle rachis are located on the short arm of Chromosome 3, being close to the map position of weak rachis locus Hst-3. Because of its similarities in terms of allelic properties and map positions to weak rachis, non-brittle rachis is a difficult trait for genetic analysis.Non-brittle rachis is a well-studied trait. Takahashi (1955) reported that brittleness was controlled by two complementary genes, which are now designated btr1 and btr2 (Franckowiak and Konishi 1996a,b). Both loci are on Chromosome 3 and semi-allelic to each other, i.e. they are tightly linked. These two loci are sometimes called btr1btr2 complex. Since all barley varieties of cultivated species H. vulgare L. subsp.vulgare have one of the two btr genes in recessive form (Takahashi 1964), the non-brittle rachis trait is not found in cultivated barley varieties but is observed in the F1 of some intervarietal crosses in which alternating btr1 and btr2 alleles are involved. H. vulgare subsp. spontaneum carries dominant forms of both btr1 and btr2, and has brittle rachis. Takahashi (1955) reported that in F2 progeny of a H. vulgare subsp. spontaneum×H. vulgare subsp. vulgare cross only one of the linked btr genes segregated and a 3 brittle: 1 tough (non-brittle) ratio occurred. However, there have also been reports of 9 brittle:7 tough ratio (Johnson and Aberg 1943; Turcotte 1957) which indicate independent segregation. Segregation ratios that did not fit the two complementary gene models have also been reported (Smith 1951). All these reports might indicate that non-brittle rachis is a trait controlled by multiple genes interacting with each other to control the trait.Developing recombinant inbred lines (RILs) in the progeny of genotypes with alternating btr1btr2 alleles and using mostly AFLP markers, Komatsuda and Mano (2002) mapped btr1 in a 7.3 cM interval flanked by e14.m27.4.1 and e15m19.7 markers on the short arm of Chromosome 3 approximately 44.5 cM from telomere and 12.0 cM from centromere. The map position of btr1 was located about 9.6 cM proximal to RFLP marker ABG471. They failed to map btr2 using the same approach. They hypothesized that the reason for this failure was the intervention of an unlinked inhibitor gene, designated D, which prevented brittleness in dd condition. Data from a limited number of RILs showed that D locus is in an approximately 30 cM interval of e15m28.7.2-e15m19.6 on chromosome 1(7H) (Mano et al. 2001). Schieman (1921) also reported an inhibitor gene for non-brittle rachis. Thus, there is convincing evidence for the presence of loci other than btr1/btr2 involved in non-brittle rachis.Our ultimate goal is to reveal the interesting head shattering system in barley using one-step-at-a-time approach. We already explained the weak rachis mechanism and mapped the major loci responsible (Kandemir et al. 2000). Although map position of btr1 was reported by Komatsuda and Mano (2002) using AFLP markers, this data needed to be clarified using more robust RFLP markers which allow better comparisons among different barley maps. Specific objectives in the present study were; 1) to clarify the position of two tightly linked non-brittle rachis loci btr1btr2 complex on the short arm of Chromosome 3 using RFLP markers, and 2) to investigate the presence of additional genes involved in non-brittle rachis.