Chapter 5 Genetic Analysis of Apomixis - cimmyt

102 1010. G.(arma.was developed in 1994 by the author whileattempting to reconcile simple inheritance forapomixis (the prevailing opinion at the time;Nogler 1984; Asker and Jerling 1992; Mogie1992) with (i) the many apparent asynchronousreplacements, competitions, andduplications of discrete developmentalsegments in reproductiveIy-anomalousspecies (Figure 7.1; many phenomena inaddition to embryo-sac induction), and (ii) thefact that nearly all apomicts are polyploid. Theauthor concluded that such a reconciliation isunreasonable. According to HFA theory,apomixis occurs when hybrids are producedfrom ecotypes that are distinctly divergentwith respect to their start times and rates ofMMC formation, meiosis, embryo sacformation, and embryogenesis relative to grossovule development. Such "genome collisions"(terminology suggested by Sven Asker,personal comm., 1997) explaill the abundantduplicity and asynchrony of developmentdepicted in Figure 7.1.In 1994, the author conducted a preliminarysearch of the literature to determine ifpolysporic and polyembryonic species containmultiple genomes, i.e., whether they arepolyploid. A negative result was soonobtained, which seemed to deal a fatal blowto this fledgling multi-genome "asynchronyhypothesis." However, in studying thegenome composition of the polysporic andpolyembryonic diploids, it was found thatthese "diploids" generally have highchromosome base numbers indicative ofpaleopolyploidy. The author concluded thatif the HFA theory is correct, the base numbertrends observed in the preliminary 1994 studyshould hold in a large-scale study of all knownapomictic, polysporic, and polyembryonicspecies. The theory survived the large-scaleexamination, was refined, and additionalhypotheses concerning the origins of apomixisand its role in the evolution of somereproductively-novel polysporic andpolyembryonic species and genera weredeveloped (Carman 1997; Peel et al. 1997a, b).The HFA theory states (i) duplicate sets ofgenes encoding female developmentalpathways exist in interracial or interspecifichybrids, polyploids, mesopolyploids, andpaleopolyploids; (ii) polygenic "heterozygosity"for photoperiodic floral induction andstart times and durations of MMC formation,megasporogenesis, embryo-sac formation,endosperm formation, and embryony, is theprimary cause of apomixis, pOlyspory,polyembryony, and related anomalies; (iii)allopolyploidy or segmental allopolyploidy isoften required for apomixis because it preventsor greatly reduces the incidence of geneticrecombination between genomically-isolatedsets of parental genes, which otherwise wouldlead to recombination among the many genesrequired for apomixis, resulting in reversionto sexuality (Carman, in preparation); (iv)polyploidy also influences apomixis byinfluencing the timing and duration of meiosis(Bennett 1977) and because divergent genomesare probably more prone to be physicallypartitioned in the nucleus (Leitch et al. 1990)when present as homologous pairs and thusmore functionally independent (Carman1997); and (v) mutations are of secondaryimportance and may improve reproductivefitness through null-allele formation in one orboth genomes. This theory is consistent withcurrent models of developmental geneexpression, including (i) the ABC model, inwhich floral genes from a B cassette areexpressed only when genes from an A cassetteare expressed (the expression of C genesrequires expression of B genes, etc.) (Theissenet al. 2000), and (ii) checkpoint models, inwhich precocious expression of checkpointgenes causes developmental phases to beskipped, e.g., fusing G]-phase yeast cells withM-phase cells causes G] nuclei of