Abstract

The foundation of western civilisation owes much to the high fertility of hexaploid (bread) wheat, which results from the stabilisation of its polyploid genome. Despite possessing multiple sets of diploid chromosomes, hexaploid wheat behaves as a diploid at meiosis, with the Ph1 locus promoting the correct pairing of homologous chromosomes. In hybrids of wheat with wild relatives, Ph1 prevents pairing and recombination between the different chromosomes. This failure in chromosome exchange prevents breeders from exploiting the diversity of wild relatives within their programmes.

The cell biology studies reveal that Ph1 is a master regulator of wheat premeiosis and meiosis, through its ability to control chromatin structure, replication, meiotic gene expression, chromosome pairing and recombination.

Mapping Ph1 has been complicated by the absence of allelic variation, being only possible to score for its presence or absence, thereby excluding conventional mapping approaches. The strategy to identify Ph1 involved the deployment of the rice synteny concept, the physical contiging of 7Mb of the wheat genome, generation of 8 mutagenised populations and the individual screening of some 50,000 mutant lines. This represented more than 30 man-years of work.

This study defined Ph1 to region containing a gene complex disrupted by a piece of sub-telomeric heterochromatin. The Ph1 gene has homology to a mammalian gene at the core of regulating replication through controlling chromatin structure. This year, researchers have shown that this mammalian gene has, as they describe, an “unpredicted” role in meiosis. It also controls chromosome pairing and recombination, thereby suggesting that it too has a major regulatory role in controlling key events during premeiosis and meiosis. The fundamental mechanisms of recognizing homologous chromosomes in meiosis are therefore likely to be conserved in mammals and plants. Thus pre-existing mechanisms have been modified in plants to deal with the additional problems encountered due to genome size and polyploidy. We have now exploited this information using a drug which regulates the mammalian gene, to also regulate Ph1 which will be of practical benefit to breeding programmes.