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Department of Biology, University of Kentucky, Lexington, Kentucky 40506
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ABSTRACT |
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 TOP ABSTRACT LITERATURE CITED |
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A genetic analysis of plasmodial fusion in the CR 10 isolate of Didymium squamulosum indicated that this isolate was heterozygous for two fusion loci. These loci display dominant and recessive alleles, and any two plasmodia must be phenotypically identical for these loci before they will fuse.
Key words: cytotoxic, self recognition, somatic incompatibility
The genetic control of plasmodial (somatic cell) fusion has thus far been studied in three species of myxomycetes—Didymium iridis (Ditmar) Fries, Physarum cinereum Schum., and Physarum polycephalum Schw. (Carlile and Dee 1967
, Collins and Clark 1968, Poulter and Dee 1968, Collins and Haskins 1970, 1972, Carlile 1973, Clark and Collins 1973a, b, Ling and Ling 1974, Clark 1977, Ling and Clark 1981). The report of plasmodial fusion in the Ky 1 isolate of Didymium nigripes (Link) Fries by Clark and Collins (1978) is no longer valid since this isolate is now considered to be the A2 biological species of D. iridis. Basically, the somatic cell reactions in these myxomycetes are controlled by polygenic systems displaying simple dominance in the diploid plasmodium. Phenotypically dissimilar plasmodia do not fuse at all or else they undergo temporary fusions that are quickly terminated by cytotoxic reactions, whereas phenotypically similar plasmodia undergo fusions that are not followed by such reactions. Although the cytotoxic reactions seem to be rarer and slower in Physarum polycephalum (Carlile 1973), and one of the loci in this species is reported to have codominant alleles (Poulter and Dee 1968), there appears to be a distinct, well-defined system of incompatibility in the myxomycetes. This study described herein was designed to extend our knowledge of myxomycete incompatibility systems to a fourth species, Didymium squamulosum (Alb. & Schw.) Fries, to provide further support for generalizations concerning these systems.
The CR 10 isolate (ElHage et al 2000) of Didymium squamulosum, collected on banana leaf litter from a plantation near Cahuita on the northwestern coast of Costa Rica, was investigated, and the methods used follow those described by Clark and Collins (1973a, b). In short, the diplo-haplontic life cycle of the myxomycetes, in which the haploid stage is represented by clonal populations of cells that can act as gametes, allows the back-crossing of F1 clones (gametes) to the original haploid parental clones. It is this type of back-crossing that makes the study of polygenic systems practical. Plasmodia obtained from crossing the parent haploid gametic clones 1 and 16 (mating type A11) against clones 4 and 5 (mating type A12) were used as starting material. These plasmodia were designated 1.4, 1.5, 16.4, and 16.5, respectively, to indicate their origin. F1 haploid clones derived from a diploid F1 plasmodium such as 1.4 were assigned numbers (e.g., 1.4–1, 1.4–2, etc.), and a plasmodium resulting from a backcross of an F1 clone to a parent (e.g., clone 1) was indicated by the designations 1.4–1 x 1, 1.4–2 x 1, and so on.
When F1 haploid clones of the appropriate mating type (A12) from the 1.4 plasmodium were backcrossed to the parent clone 1 (mating type A11), the resulting plasmodia were of two fusion classes (classes I and II; fusion classes are groups of plasmodia that fuse within but not between classes), and when the A11 mating type F1 clones were crossed to parent clone 4 (mating type A12) they also produced two (I and III) fusion classes (Table I). Since the only fusion class (I) the two sets of backcross plasmodia have in common when they are tested against each other is the same as that of the 1.4 plasmodium, the existence of two loci is required to explain the results. The 1.4 plasmodium can be assigned the genotype I1/i1–i2/I2 (Table II). The letters above the lines refer to alleles contributed by parent clone 1 whereas those below the lines are derived from parent clone 4. Assuming dominance, the 1.4 plasmodium has a I1–I2 phenotype and defines one (I) fusion class. The other two fusion classes would be I1–i2 (class II; backcrosses to parent clone 1, which has a dominant I1 allele, that are not I1–I2) and i1–I2 (class III; backcrosses to parent clone 4, which has a dominant I2 allele, that are not I1–I2).
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When the four fusion phenotypes (I1–I2, I1–i2, i1–I2, and i1–i2) were tested for cytotoxic reactions (a transient fusion is followed by the intermixed area losing pigment, becoming highly vacuolate and being delimited from the rest of the plasmodium by a membrane) by pairing them in all possible two-way combinations, it was observed that each locus produced a lysed zone of characteristic size. When two plasmodia differed only at the I1 locus, the plasmodium displaying the dominant phenotype caused a killed zone of 0.1 units (see Clark and Collins 1973b for rationale and derivation of killed zone units) in the plasmodium carrying the recessive phenotype. Similarly, the dominant I2 phenotype caused a 0.2 killed zone in the recessive phenotype. However, both loci acting together (one plasmodium being dominant and the other recessive at both loci) produced a killed zone of 0.05 units. The smaller the killed zone, the stronger the incompatibility reaction (Clark and Collins 1973b) in that very fast (strong) reactions kill the mixed cytoplasmic regions before the zone can become extensive, while slow (weak) reactions allow considerable mixing before the cytotoxic reaction occurs. Also, the loci are additive in that the killed zone is smaller when both loci are active than it is for either locus alone. The biological nature of the killing reaction is unknown, although a similar slow (24 h) acting heterokaryon incompatibility system in Physarum polycephalum, where one of the sets of nuclei are lysed, requires the de novo synthesis of high molecular weight compounds (Schrauwen 1979).
The data obtained in the present study indicate that plasmodial fusion in the CR 10 isolate of Didymium squamulosum is controlled by a two loci polygenic system displaying dominant and recessive alleles. Plasmodia will not fuse successfully unless they are phenotypically identical at both loci, since dissimilar phenotypes for either or both loci produce a cytotoxic reaction resulting in the lysis of any mixed cytoplasm produced by a temporary fusion. These results conform to those already found in the other species studied (Collins and Haskins 1972, Clark and Collins 1973a, b, Clark 1977).
The maintenance of individuality in an organism depends upon a system of self /non-self recognition, which appears to be a fundamental characteristic of biological organization. Such a system is especially critical in the myxomycetes, where auto-fusion of different portions of the same plasmodium is an integral function of cell behavior that also precludes any physical barriers to fusion in this group. For this reason, comparative studies of self /non-self recognition in the myxomycetes, in which there is a well-defined system, contribute to the general advancement of the basic question of biological individuality.
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FOOTNOTES |
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Accepted for publication May 24, 2002.
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LITERATURE CITED |
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TOPABSTRACTLITERATURE CITED |
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———, Dee J., 1967 Plasmodial fusion and lethal interactions between strains in a myxomycete. Nature 215:832-834[Medline]
Clark J., 1977 Plasmodial incompatibility reactions in the true slime mold Physarum cinereum. Mycologia 69:46-52
———, Collins OR., 1973a Further studies on the genetics of plasmodial incompatibility in a Honduran isolate of Didymium iridis. Mycologia 65:507-518
———, ———. 1973b Directional cytotoxic reactions between incompatible plasmodia of Didymium iridis. Genetics 73:247-257
———, ———. 1978 Plasmodial incompatibility in the myxomycete Didymium nigripes. Mycologia 70:1249-1253
Collins OR, Clark J., 1968 Genetics of plasmodial incompatibility and heterokaryosis in Didymium iridis. Mycologia 60:90-103
———, Haskins EF., 1970 Evidence for polygenic control of plasmodial fusion in Physarum polycephalum. Nature 226:279-280[Medline]
———, ———. 1972 Genetics of somatic fusion in Physarum polycephalum: the PpII strain. Genetics 71:63-71
ElHage N, Little C, Clark J, Stephenson SL., 2000 Biosystematics of the Didymium squamulosum complex. Mycologia 92:54-64
Ling H, Clark J., 1981 Somatic cell incompatibility in Didymium iridis: locus identification and function. Amer J Bot 68:1191-1199
———, Ling M., 1974 Genetic control of somatic cell fusion in a myxomycete. Heredity 32:95-104[Medline]
Poulter RTM, Dee J., 1968 Segregation of factors controlling fusion between plasmodia of the true slime mould Physarum polycephalum. Genet Res 12:71-79[Medline]
Schrauwen J., 1979 Post-fusion incompatibility in Physarum polycephalum. Arch Microbiol 122:1-7
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