Chapter 5 Genetic Analysis of Apomixis - cimmyt

104 J... G.(.....effects), which could be caused by differencesin genetic background, or (ii) envirorunentalfactors that reduce the degree of asynchronyby accelerating or decelerating geneexpression from one genome relative to thatof another (photoperiod or temperatureresponses, e.g., as occurs in Dicanthium,Themedtl), thus allowing sexual developmentto occur facultatively (Carman 2000).According to the HFA theory, polyspory andpolyembryony result from the competitiveexpression of grossly imbalanced genomes(incompletely duplicated sets of reproductivegenes) in which some checkpoint systems aremissing. In contrast, competitive expressionamong genomes is terminated by checkpointgenes in apomicts, which generally containbalanced sets of reproductive genes (Carman1997), thus allowing a somewhat smoothtransition to apomixis (Figure 7.2).Apomixis is much more prevalent amongoutcrossing species than inbreeding species(Asker and Jerling 1992). This is consistentwith the HFA theory because outcrossingspecies are much more prone to forminterecotypic or interspecific polyploids whensecondary contacts occur, e.g., during thenumerous major. climatic shifts associated withthe Pleistocene glaciations (Frakes et al. 1992;Carman 2000). Likewise, more apomicts arealiopolyploid than autopolyploid becausepolyploidization by Bill hybrid formation isexpected to occur more frequently in naturein interspecific hybrids than interracialhybrids. Similarly, the chances of Bill hybridformation occurring in interecotypic orinterspecific F 1hybrids that are sterile andannual are low compared to their formationin sterile perennials, which may flowerannually for many years. This factor limits thechances of annuals becoming apomictic andexplains their low frequency in nature.The HFA theory also predicts ambiguousoutcomes regarding the sexuality of progenywhen an apomict is crossed with a sexual orwith another apomict, regardless of thecloseness or wideness of the cross. The modeof reproduction expressed in the progeny willdepend on how the added or removedgenome(s) affect asynchrony, and this cannotbe predicted without some a priori knowledgeof the female developmental schedulesencoded by the involved genomes (Carman1997). That these many inconsistencies in theapomixis literature are explained by the HFAtheory is strong evidence for its validity.Testing the Gene EffectHypothesesIf apomixis is the result of one or a fewmutations, similar artificially inducedmutations might produce apomicts fromsexual species. Research programs currentlyexploring this possibility are reviewed byBicknell (Chap. 8), Grossniklaus (Chap. 12),and Praekelt and Scott (Chap. 13). Likewise,simple inheritance should permit transfer ofapomixis gene(s) to sexual species. To date,introgression projects have failed to conferapomixis upon sexual species by addinganything less than at least one complete alienchromosome (Savidan, Chap 11). Kindiger etal. (1996) reported a condition that might leadto an exception. They isolated, from theirmaize-Tripsacum backcross program, a line (30Mz + 9 Tr chromosomes) that appears tocontain a maize Tripsacum translocationpossessing gene(s) for apomixis. However,Blakey et al. (1997, reviewed below)determined that the genes required forapomixis occur in five distinct Tripsacumlinkage groups that are syntenic to regions onthree maize chromosomes. These data castdoubt on Kindiger's simple inheritance model.