Chapter 5 Genetic Analysis of Apomixis - cimmyt

From Su.oIily '0 Apomixis: MoJ...lar .nd Gen.t. Appr••d,•• 179compatible with it. Several models thatconsider the relationship between polyploidyand apomixis have been put forward (Nogler1982; Mogie 1992; Noirot 1993; Carman 1997;Grimanelli et al., Chap. 6). For instance, anal teration of cell cycle length as hypothesizedabove may be caused by polyploidization orwide hybridization. In many species withisolates of several ploidy levels, diploids areusually sexual and polyploids apomictic(Asker and Jerling 1992; Leblanc et al. 1995).Autoploidization of sexual diploids hasresuIted in apomictic tetraploid plants in somespecies (Burton 1992). It is attractive tospeculate that the cell cycle length is altered inresponse to changes in ploidy. However, noexperimental data is available to support thishypothesis since essentially nothing is knownabout the regulation of the cell cycle duringreproductive development in plants. Theassociation of polyploidy with apomixis may,however, be a secondary effect caused bydeleterious mutations that accumulated in thegenome of apomicts. This is supported by therecent isolation of diploid apomicts inHierncium and Allium (Bicknell 1997; Kojimaand Nagato 1997). These and earlier findingssuggest that polyploidy is not an absoluterequirement for apomixis (Savidan 1980;Nogler 1982; Hashemi et al. 1989).An attractive hypothesis, which takes bothdevelopmental and genomic peculiarities intoaccount, has recently been proposed byCarman (1997; Chap. 7) based on earliermodels put forward by Ernst (1918). In short,the duplicate-gene asynchrony hypothesisstates that duplicate sets of genes regulatingreproductive development exist in polyploids.Polyploidy originally arose throughhybridization, such that the regulatory controlof development originating from the twogenomes may not be in synchrony. Theresulting intergenomic regulatory conflict maythen lead to the developmental aberrationsobserved in apomicts and other reproductiveanomalies. An important aspect of this theoryis that apomixis results from the conflictingaction of genes that usually playa regulatoryrole during sexual development, i.e., the samewild-type genes (not mutant forms) controlboth sexuality and apomixis. This reinforcesthe need for a better understanding of themolecular and genetic basis of sexualreproduction for the engineering of apomixisin sexual crops.Another consideration that could influenceresearch strategies was raised by Jefferson andBicknell (1996). At present, there is no evidenceto indicate that apomixis is controlled by atrans-acting gene product rather than by a cisactingelement. One can envision an alterationof a cis-acting element, for instance a bindingsite for a trans-acting factor (e.g., for atranscription factor or chromatin component),with altered affinity or copy number that couldcause apomixis by changing the concentrationof the trans-acting factor in the cell. Forexample, the factor could be titrated out by anincrease in the copy number of its binding sites,which in turn would result in precocious orinappropriate development of the embryo sac.Thus, a dominant locus could readily beexplained. The recent observation that largegenomic regions that are associated with theinheritance of apomixis are not present insexual relatives (Ozias-Akins et al. 1998; Rocheet al. 1999) is consistent with such a mechanism.Genetic Control ofReproduction and CandidateGenes for the Engineering ofApomixisTo date, no fully apomictic mutants have beenrecovered in sexual species, however, severalmutants and spontaneously occurringvariations of sexual reproduction displayindividual components of apomixis. Theseinclude the production of unreduced spores