Genetic mechanisms of apomixis.
The introduction of apomixis to crops would allow desirable genotypes to be propagated while preventing undesirable gene flow, but so far there has been little success in transferring this trait from a natural apomict to another species. One explanation is the sensitivity of endosperm to changes in relative maternal and paternal contribution owing to parental imprinting, an epigenetic system of transcriptional regulation by which some genes are expressed from only the maternally or paternally contributed allele. In sexual species, endosperm typically requires a ratio of two maternal genomes to one paternal genome for normal development, but this ratio is often altered in apomicts, suggesting that the imprinting system is altered as well. We present evidence that modification of DNA methylation is one mechanism by which the imprinting system could be altered to allow endosperm development in apomicts. Another feature of natural apomixis is the modification of the normal fertilization programme. Sexual reproduction uses both sperm from each pollen grain, but pseudogamous apomicts, which require a sexual endosperm to support the asexual embryo, often use just one. We present evidence that multiple fertilization of the central cell is possible in Arabidopsis thaliana, suggesting that pseudogamous apomicts may also need to acquire a mechanism for preventing more than one sperm from contributing to the endosperm. We conclude that strategies to transfer apomixis to crop species should take account of endosperm development and particularly its sensitivity to parental imprinting, as well as the mechanism of fertilization.
Spielman
Melissa
M
Department of Biology and Biochemistry, University of Bath, Claverton Down, Bath BA2 7AY, UK.
Vinkenoog
Rinke
R
Scott
Rod J
RJ
D005075:Biological Evolution; D018556:Crops, Agricultural / Q000235:genetics / Q000502:physiology; D005818:Genetic Engineering; D019684:Magnoliopsida / Q000235:genetics* / Q000502:physiology*; D012100:Reproduction, Asexual / Q000235:genetics* / Q000502:physiology*