Abnormal Phenotypes in Wheat Hybrids
Wheat type I necrosis, caused by Ne1-Ne2 complementary genes, is a good example of a DM incompatibility (Tsunewaki 1960). Necrotic cell death induced by the Ne1-Ne2 epistatic interaction is accompanied with generation of reactive oxygen (Sugie et al. 2007). Because the Ne2 gene seems to be located in a chromosomal region closely linked to the R gene against rust fungus, it has been postulated that type I necrosis is due to autoimmune-like responses triggered by the Ne1-Ne2 interaction (Bomblies and Weigel 2007). The Ne1-Ne2 interaction results in segregation distortion of molecular markers around the Ne1 and Ne2 chromosomal regions in mapping populations of common wheat even if the necrotic effect is weak (Takumi et al. 2013; Iehisa et al. 2014).
Sometimes ABD triploid hybrids between tetraploid wheat and wild diploid Aegilops tauschii Coss. show abnormal growth phenotypes such as germination failure, hybrid necrosis and hybrid sterility (Matsuoka et al. 2007). In particular, the abnormal growth phenotypes in hybrids between the tetraploid wheat cultivar Langdon and Ae. tauschii accessions have mainly been divided into the following four types: two types of hybrid necrosis (type II and type III), hybrid chlorosis, and severe growth abortion (Mizuno et al. 2010). In hybrid lines showing type III necrosis, cell death occurs, gradually beginning with older tissues, as observed in type I necrosis. Type III necrosis is presumed to be due to interaction of Nec1 and Nec2 complementary genes located on the D and AB genomes, respectively. Plants exhibiting type II necrosis show necrotic symptom and marked growth repression only under low temperature. A previous report assumed that complementary genes located on the AB and D genomes, respectively named Net1 and Net2, trigger type II necrosis (Nishikawa 1962). A hypersensitive response-like reaction might be associated with necrotic cell death in type II and III necrosis (Mizuno et al. 2010, 2011). Therefore, the two types of hybrid necrosis in wheat triploid hybrids at least partly share similar responses.
In addition to necrotic symptom, a significant decrease in cell cycleand divisionrelated gene expression occurs at the crown tissues including the shoot apical meristem (SAM) of plants displaying type II necrosis (Mizuno et al. 2011). Severe growth abortion, which is hybrid lethality with developmental arrest at the early seedling stage in ABD wheat hybrids, might be caused by abortion of mitotic cell division and meristematic activity at the SAM (Hatano et al. 2012). In severe growth abortion, the related cell death induced by an autoimmune response might be a secondary event; arrest of cell division at SAM seems to occur prior to the autoimmune response (Hatano et al. 2012). Thus, dramatic alteration of gene expression profiles at the SAM induced by the AB and D genome interaction could be significantly associated with the growth abnormalities in triploid wheat hybrids.
Interestingly, tiller number is dramatically increased at normal temperatures in type II necrosis, although plant height is significantly shorter (Mizuno et al. 2011). An extremely bushy dwarf phenotype, called grass clump, can also be induced by epistatic interaction of Net1 and Net2. Therefore, phenotypic effects of the Net1Net2 interaction at the crown tissues show plasticity strongly dependent on plant growth temperature (Takumi and Mizuno 2011; Fig. 17.1). At the normal growth temperature, transcriptome analysis of the crown tissues of plants with type II necrosis showed downregulation of wheat APETALA1-like MADS-box genes, which are considered to act as flowering promoters (Matsuda et al. in preparation). The downregulation of the MADS-box genes corresponds with the delayed flowering phenotype in plants showing type II necrosis. On the other hand, disease resistance-related genes are not upregulated under normal temperature conditions (Matsuda et al. in preparation). Thus, dramatic alteration of gene expression profiles at the SAM induced by DM gene interaction could be significantly associated with the growth abnormalities in triploid wheat hybrids.
Fig. 17.1 Putative mechanism underlying the temperature-dependent phenotypic plasticity observed in ABD wheat hybrids