POLYPLOIDY AND DIPLOIDY: NEW PERSPECTIVES ON CHROMOSOME PAIRING AND ITS EVOLUTIONARY IMPLICATIONS

The last widely accepted classification of polyploidy recognized three major categories: autoploidy, segmental alloploidy, and true alloploidy. Criteria for recognizing these types were based largely on chromosome pairing in F1 hybrids, but until very recently there were no quantitative criteria to distinguish autoploids from segmental alloploids. This is theoretically possible, and Jackson and Casey (1982) and Jackson and Hauber (1982) have presented models and methods to quantitatively predict the frequencies of the different meiotic configurations in autotriploids through autooctoploids. The expected numbers of configurations then can be statistically tested for goodness of fit with observed data. Synthetic and natural autotetraploids have been shown to fit the models well. However, the exceptions that do not fit are of particular interest because they indicate the presence of Ph-like (Pairing homoeologous) genes that cause fewer multivalents and more bivalents than expected in the autoploid models. The effect of Ph-like genes at the nuclear level apparently involves placement of chromosome attachment sites on the nuclear membrane such that different genomes occupy slightly different sites. This would be far enough apart in true alloploids so that no pairing occurred in the original F1 hybrid. In true autoploids and normal diploids, homologues are equally close so that pairing obeys probability laws that make it possible to describe expected pairing events with appropriate models and equations. From the foregoing statements, one can deduce that the terms autoploid, segmental alloploid, and true alloploid need not and indeed should not be equated with results of crosses between any taxonomic levels. Rather, they represent conditions that can be attained by one or very few genes acting on nuclear membrane attachment sites. It is possible to deduce from hybrids at the diploid level the type of polyploid that can be obtained, and such data can have great agronomic value. A generally held dogma is that the inability of chromosomes to pair in F1 hybrids is due to considerable genetic divergence and perhaps numerous structural changes at the light microscope and/or ultrastructural level. Data from various sources show that this need not be true, and there is no reason to believe this is a factor in what has been called genome divergence in the classical sense. Genome divergence in terms of pairing ability can occur at the population level due to one or a few genes. THE LAST WIDELY ACCEPTED classification of polyploidy was by Stebbins (1947) who recognized three major categories: autopolyploids, segmental allopolyploids, and true allopolyploids. The basis for distinguishing these types was the behavior of chromosomes in individuals and F1 hybrids. Intrapopulation diploids were expected to exhibit normal chromosome pairing, but F1 hybrids between parents of various degrees of genetic divergence would show appropriate reduction in I Received and accepted for publication 16 August 1981. This paper is based on a lecture presented at the symposium on "Frontiers of Plant Genetics" sponsored by the Genetics Section of the Botanical Society of America and held at Indiana University in August, 1981. I thank Brian Murray, Donald Hauber, and Paul Grun for their helpful comments and criticisms. pairing. A major cause of divergence was believed to be structural alterations such as translocations, inversions, duplications, deletions, transpositions, cryptic structural differences, or other unobserved and unknown causes. The cryptic structural differences in the original sense (Stebbins, 1945) were cryptic mainly because meiotic analyses were usually limited to diakinesis or later stages; pachytene stages were not analyzed. Thus chromosome associations at post pachytene stages such as diakinesis or metaphase I in F1 hybrids was a major criterion for distinguishing the type of polyploid that would be produced, and there was the explicit or at least the tacit assumption that lack of pairing in diploids and in polypoids was due to lack of homology caused principally by gross structural alterations of the chromosomes.