Dr Bill Finch-Savage
Most seeds are well equipped to survive extended periods of unfavourable conditions for germination. At least in part, this ability stems from the evolution of a wide range of dormancy mechanisms. Physiological seed dormancy is present throughout the higher plants and has a profound impact on the timing and periodicity of weed seedling emergence and more widely in the structure and development of plant communities across all major climatic regions.The induction and loss of dormancy are triggered by diverse environmental cues activated through many different physiological mechanisms. Yet the function of dormancy is remarkably similar across species, i.e. to spread germination across time, but in synchrony with seasonal cycles to avoid unfavourable weather, to maximise competitive advantage, and to ensure the establishment of plants.
There is considerable ignorance of how dormancy is controlled at the molecular level and this hampers the development of more efficient practices in crop production, ex situ genetic conservation and habitat creation and restoration. In order to gain greater understanding of the molecular basis of seed dormancy we have used full genome microarrays to conduct a global transcript analysis of Arabidopsis thaliana (accession Cvi) seeds in a range of dormant and dry-after-ripened states during cycling (Cadman et al., 2006. The Plant Journal, 46:805-822). Principal component analysis of the expression patterns observed showed that they differed in newly imbibed primary dormant seeds, as commonly used in experimental studies, compared with those in the maintained primary and secondary dormant states that exist during cycling. Dormant and after-ripened seeds appear to have equally active although distinct gene expression programmes, dormant seeds having greatly reduced gene expression associated with protein synthesis, potentially controlling the completion of germination. A core set of 442 genes were identified that had higher expression in all dormant states compared with after-ripened states. Abscisic acid (ABA) responsive elements were significantly over-represented in this set of genes the expression of which was enhanced when multiple copies of the elements were present. ABA regulation of dormancy was further supported by expression patterns of key genes in ABA synthesis/catabolism, and dormancy loss in the presence of fluridone. The data support an ABA–gibberelic acid hormone balance mechanism controlling cycling through dormant states that depends on synthetic and catabolic pathways of both hormones.
The depth of seed dormancy can be influenced by a number of different environmental signals, but it has yet to be investigated whether a common mechanism underlies this apparently similar response. Full-genome microarrays were also used for a global transcript analysis of Arabidopsis seeds exposed to dry after-ripening (AR), low temperature stratification, nitrate and light (Finch-Savage et al., 2007; The Plant Journal 51: 60-78). Germination studies showed that the sensitivity of seeds to low temperature, nitrate and light was dependant upon the length of time spent AR following harvest. Seeds had an absolute requirement for light to complete dormancy release in all conditions, but this effect required an exposure to a prior dormancy relieving environment. Principal component analyses of the expression patterns observed grouped physiological states in a way that related to the depth of seed dormancy, rather than the type of environmental exposure. Furthermore, opposite changes in transcript abundance of genes in sets associated with dormancy or dormancy relief through AR were also related to the depth of dormancy and common to different environments. Besides these common quantitative changes, environment-specific gene expression patterns during dormancy relief are also described.
The results of both studies (Cadman et al., 2006; Finch-Savage et al., 2007) are consistent with a role for an ABA-gibberellic acid balance in integrating dormancy-relieving environmental signals (see figure below). The combined data sets are available on the following web sites:
In a recent review (Finch-Savage and Leubner-Metzger, 2006. New Phytologist, 71:501-523) we have presented an integrated view of the evolution, molecular genetics, physiology, biochemistry, ecology and modelling of seed dormancy mechanisms and their control of germination. We argue that adaptation has taken place on a theme rather than via fundamentally different paths and identify similarities underlying the extensive diversity in the dormancy response to the environment that controls germination.
Model for the regulation of dormancy and germination by ABA and GA in response to the environment. According to this model ambient environmental factors (e.g. temperature) affect the ABA/GA balance and the sensitivity to these hormones. ABA synthesis and signalling (GA catabolism) dominates the dormant state, whereas, GA synthesis and signalling ( ABA catabolism) dominates the transition to germination. The complex interplay between hormone synthesis, degradation and sensitivities in response to ambient environmental conditions can result in dormancy cycling. Change in the depth of dormancy alters the requirements for germination (sensitivity to the germination environment); when these overlap with changing ambient conditions, germination will proceed to completion. Model based on work with A. thaliana ecotype Cvi, modified from Cadman et al. (2006). Key target genes are in parenthesis.
Figure published in the Tansley review "Seed dormancy and the control of germination" by Finch-Savage WE and Leubner-Metzger G
(New Phytologist 171: 2006)
A PDF file of this review is available for download from the New Phytologist Trust website at New Phytologist Trust - Tansley Reviews
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