Pre-harvest sprouting (PHS) in wheat causes downgrading of grain quality, severely limits end-use applications and results in substantial financial losses to farmers and food processors. Tolerance to PHS is therefore a highly desirable but complex trait sought by plant breeders. The overall resistance to sprouting damage results from a combination of factors influencing water uptake and drying rate of the ear, grain dormancy and the mobilisation of storage reserves to support germination. These processes are regulated by a number of key resistance genes that interact strongly with environmental conditions.
A major component of the observed genetic variation in sprouting of grains within the ear is the degree of embryo dormancy at grain harvest. By dormancy we simply mean that germination of the embryo does not occur even when grains are placed under otherwise favourable conditions of moisture and warmth. Environmental conditions during grain development, the temperature used to test germination, and the stage of grain maturity, all affect the degree of embryo dormancy. In general, more dormant grain is produced under cool growing conditions whereas high temperatures during the later stages of grain growth break embryo dormancy allowing grains to germinate in the ear if rain occurs around harvest time. It is also important to appreciate that individual grains within an ear may have different basal response thresholds to water availability and hormonal signals. In other words, only a proportion of the population of grains within an ear, and ears within a crop, may exhibit the phenomenon of PHS.
In the UK and other regions of the world, certain seasons are worse than others for the prevalence of PHS. According to the HGCA Harvest Quality Survey for 1999, the UK wheat harvest was 'problematic with whole swathes of grain losing their milling quality all over the southern and eastern part of the country'. As the Survey states, 'ripe grain fell prey to high temperatures and heavy rain', causing sprouting in the ear and low Hagberg falling numbers (a measure of the viscosity of a suspension of flour). The main cause of low Hagberg falling number is the presence of high a-amylase activity in flour, resulting in the degradation of starch to simple sugars that cause 'sticky crumb' structure of bread loaves and caramelisation of the crust during the baking process.
When the grain reaches maximum size, about 3-4 weeks after flowering, there follows a net loss of water from the grain and the ripening process begins. The cells of the starchy endosperm start to die but those of the aleurone layer and the embryo remain viable. The mechanism by which these cells survive involves the synthesis of a range of protective proteins that allow cells to tolerate desiccation. The loss of water from cells also acts as an important signal inducing developmental arrest and a state of dormancy in the embryo and aleurone layer, thereby preventing the initiation of a premature germination programme. There is good evidence from developmental mutants in maize, and other plants, that the plant hormone, abscisic acid (ABA), is involved in the regulation of embryo dormancy. In wheat, no increase in ABA content is associated with the induction of dormancy but there is strong evidence that changes in ABA responsiveness are related to the maintenance of dormancy. For example, embryos isolated from wheat varieties showing strong dormancy are more responsive to ABA than those from PHS-susceptible varieties. The same is also true for grains of a given variety grown under cool conditions that induce stronger dormancy than for grains from plants grown under warmer conditions.
Normally, grains show some degree of dormancy when harvested and require a period of so-called 'after-ripening' before dormancy is broken and germination commences under favourable conditions. So why do some grains germinate prematurely whilst still in the ear? What appears to happen is that the dormancy mechanism is disrupted in some way and only a very short period of 'after-ripening' is required before grains can germinate in the ear provided sufficient moisture is present. One way to visualise this sequence of events is to imagine there is a natural switching mechanism at some point during the normal course of grain development. When the switch is ON, dormancy is induced and maintained until harvest ripeness and grains will require a period of 'after-ripening' before being able to germinate. If the switch were of a dimmer-type, the extent to which it was turned on would reflect variation in the potential degree of dormancy of different wheat varieties (genotypes). In unfavourable weather conditions (environment), the switch may be turned OFF breaking the dormancy mechanism and allowing grains to germinate prematurely in the ear if rain occurs around harvest time. Such a bypassing of the normal dormancy and after-ripening phases is a so-called 'default' pathway and suggests a potential overlap of the dormancy and germination programmes during grain development. What happens if this switch is a regulator gene that has the capacity to turn on other genes associated with the dormancy pathway and prevent grains entering the default germination pathway? How does the environment affect the expression of this regulator gene to turn off the switch and permit the default pathway that allows grains to germinate prematurely in the ear?
One reason for favouring the idea of a regulator gene that can switch grain development between the normal and default pathways arises from a mutant of maize, called viviparous 1. This mutation causes premature germination of embryos whilst still on the cob, a phenomenon very similar to that observed during pre-harvest sprouting in wheat. The non-mutant maize gene encodes a protein belonging to a class of 'transcription factors' that confers responsiveness of tissues to ABA and regulates the activity of a family of genes involved in the later stages of normal grain development. In addition, the Vp1 transcription factor also represses genes encoding hydrolytic enzymes, such as a-amylase, that are normally associated with the germination programme.
A wheat gene affecting embryo sensitivity to ABA has been mapped to the same chromosome as that of the corresponding wheat Vp1 genes, but at present it is not know if they map to precisely the same locus on chromosome 3. Recent evidence suggests that the relatively weak embryo dormancy of modern wheat varieties may be related to disrupted processing of the wheat Vp1 gene product leading to insufficient functional protein to ensure a high degree of embryo dormancy. In addition, expression of wheat Vp1 genes ceases, whereas that of germination-related genes is induced, during the final stages of grain development when plants are grown in a 'sprout-inducing' environment but not under warm, dry growing conditions. What is not known is how environmental factors affect these changes in the pattern of gene expression and whether sufficient genetic variation in responsiveness is available in seed stocks to select material with greater resistance to sprouting damage.