Chromosome 7D: Carrier of a Suppressor and a Nonsuppressor
A Suppressor of Stem Rust Resistance
Canthatch is an old Canadian hard red spring wheat cultivar that is a derivative of Thatcher (McCallum and DePauw 2008). Canthatch is susceptible to several races of Pgt and was used in many genetic studies by Dr. Eric Kerber (retired, AAFC, Winnipeg, Canada). In an early experiment, the A and B genome component of Canthatch was isolated to generate an 'extracted tetraploid' which had the genome constitution of 2n = 4x, AABB (Kerber 1964). The extracted tetraploid, named Tetra Canthatch, lacked vigour, had low fertility, and was morphologically different from Canthatch and common tetraploids. Furthermore, Tetra Canthatch had seedling resistance to some Pgt races that were virulent to Canthatch. This implied that the D genome or a component of the D genome was suppressing Sr genes present on the A and/or B genomes in Canthatch. Using nullisomic and ditelosomic stocks in a Canthatch background, it was demonstrated that the suppression of Sr genes was caused by the long arm of chromosome 7D (Kerber and Green 1980). Induced mutants showed the same phenotype as Tetra Canthatch and Canthatch ditelo 7DS. Furthermore, the suppression was caused by a single gene on chromosome 7DL (Kerber 1991). Telocentric mapping showed that the suppressor locus was independent of the centromere.
Adult-Plant Resistance Genes Can Act as a Nonsuppressor
Lr34 is a well-known adult-plant resistance (APR) gene that confers quantitative resistance to all of three of the rust disease of wheat and is located on the short arm of chromosome 7D (Dyck 1987; Singh et al. 2012). In addition to conferring APR, Lr34 was associated with nonsuppression of seedling stem rust resistance in a Thatcher background (Dyck 1987; Kerber and Aung 1999). Comparing Canthatch, Thatcher, Tetra Canthatch, Canthatch-nulli 7D and RL6058 (a Thatcher NIL carrying Lr34) with four races of Pgt, Dyck (1987) showed that (1) Canthatch and Thatcher were susceptible to all four races of Pgt, (2) Tetra Canthatch and Canthatchnulli 7D were resistant to three of these races, (3) RL6058 was resistant to the same three races as Tetra Canthatch and Canthatch-nulli 7D, and (4) one race was virulent on all five genotypes. Thus, it appears that Lr34 negates the effect of the suppressor locus and that that the stem rust resistance expressed in Thatcher-type wheats by either removing the suppressor or adding Lr34 is race-specific. Figure 20.2 shows a conceptual drawing of the relationship between the suppressor locus and Lr34, although the actual mechanisms are not presently understood.
Another Thatcher NIL, RL6077, showed the same pattern of seedling stem rust resistance as RL6058 (Dyck 1987). RL6077 carries the gene Lr67 which is similar to Lr34 in its phenotype and its multiple-disease resistance (Hiebert et al. 2010). A preliminary study showed that Lr67 was responsible for the expression of seedling stem rust resistance in RL6077 and appeared to act as a nonsuppressor like Lr34 (Hiebert et al. 2012). Thus, two unique APR genes, which both confer multiple pest resistance, also appear to act as nonsuppressors of seedling stem rust resistance genes found in Thatcher-type wheats.
We presented preliminary data in three areas to (1) assess Lr34 as a nonsuppressor,
(2) preliminary map position of seedling stem rust resistance in Thatcher expressed in the presence of Lr34, and (3) preliminary map position of stem rust resistance in the field that is expressed in the presence of Lr34. Using mutants of Lr34 in RL6058 (Spielmeyer et al. 2013), it appears that mutant lines that have lost Lr34 activity
Fig. 20.2 A conceptual summary of the interaction of the suppressor (Sup) and Lr34 on chromosome 7D. (a) The suppressor prevents the expression of seedling Sr genes from the A and/or B genomes of Thatcher-type wheats if the susceptible allele of Lr34 is present. (b) Knocking out the suppressor by mutagenesis allows the expression of the otherwise suppressed Sr genes. (c) The resistant allele of Lr34 appears to negate the effect of the suppressor and allows the expression of the Sr genes
have also lost the seedling stem rust resistance observed in the presence of a normal Lr34 allele. Thus, we tentatively claim that it is Lr34 that is responsible for the nonsupressing character observed in RL6058 and not a gene tightly linked to Lr34. We developed two populations that are fixed for Lr34 but segregate for Thatcherderived seedling stem rust resistance and resistance in the field. Seedling resistance and field resistance were mapped as QTL in these preliminary analyses and chromosome 3B significantly contributed to both traits. These preliminary findings need to be confirmed and experiments are ongoing to do so.
One aspect of the relationship between the suppressor on 7DL and Lr34 that is presently unknown is whether removing or inactivating the suppressor leads to the expression of the same Sr genes that are expressed in the presence of Lr34. Similarly, we do not know if Lr67 and Lr34 are interacting with the same genes. These lines of investigation are ongoing and should fill in the gaps in our knowledge of these interactions. From a practical standpoint, understanding these genetic interactions could be important for wheat breeders. It would easier to retain Sr genes (i.e. the suppressed genes) in elite breeding material and add, for example, Lr34 compared to the effort of introducing new or different Sr genes to enhance to stem rust resistance in new cultivars. In Canada, Thatcher comprises a large component of coefficient of parentage for most of the widely grown hard red spring wheat cultivars (McCallum and DePauw 2008). Thus, identifying the genes in Thatcher that are expressed in the presence of Lr34 is directly applicable.
An array of strategies can be employed to achieve resistance to stem rust. There is not a “one size fits all” approach that must be followed. However, genetic resources for resistance to stem rust are valuable and implementing a strategy that prolongs the usefulness of Sr genes is the responsible approach. In order to accomplish this we must understand which genes are present in our germplasm, determine the relationships between genes and their breadths of effectiveness, develop tools for molecular breeding approaches, and unravel the genetic interactions that can lead us to more durable resistance. Here we examined two examples of the lines of research that can help geneticists, pathologist and breeders reach the goal of effective and durable resistance. With the recent investment in various aspects of wheat stem rust research more tools and resources are becoming available. It is now our responsibility to translate the advances made in the lab into rust resistant wheat cultivars in the field.