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The mechanism whereby the genes M1 and M2 in Paramecium aurelia, stock 540, control growth of the mate-killer (mu) particles

Published online by Cambridge University Press:  14 April 2009

I. Gibson ,
G. H. Beale  and
E. C. R Reeve
I. Gibson
Affiliation:
Institute of Animal Genetics, Edinburgh, 9
G. H. Beale
Affiliation:
Institute of Animal Genetics, Edinburgh, 9
E. C. R Reeve
Affiliation:
Institute of Animal Genetics, Edinburgh, 9

Extract

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1. Replacement of the dominant genes M1 and M2 in Paramecium aurelia, stock 540 (syngen/variety 1), results in loss of ability to maintain mu particles and manifestation of mate-killing after a delay of eight to fifteen fissions in most cells. The change, when it does occur, is relatively abrupt, extending over less than the space of one inter-fission period.

2. The delay between change of genotype and loss of mu particles is interpreted as being due to presence in the initial cytoplasm of some thousand ‘metagons’, which are non-replicating gene derivatives having the physiological activity of the corresponding genes. During successive fissions of paramecia deprived of M1 and M2 the metagons are passively distributed amongst the progeny, until virtually all animals lack them.

3. On reaching a stage at which some individuals of genotype m1m1m2m2 contain only a single metagon, the paramecia still contain large numbers of mu particles and are mate-killers. Fission of such animals gives rise to one daughter again with mu particles, and another in which the latter are destroyed during the next inter-fission period.

4. By induced cytoplasmic exchange between conjugants, metagons can be transferred from one animal to another via the cytoplasm. Where such transference is into an animal not originally containing mu particles, that animal is converted into a condition in which it favours the maintenance of mu particles and transmits the latter to one or more of its offspring.

5. Distribution of metagons amongst progeny of dividing paramecia is not random, due possibly to clumping of the metagons. Induced cytoplasmic exchange seems to break up the clumps.

6. Reintroduction of a dominant gene (M2) into a cell recently deprived of the same gene, succeeds—even after fifteen fissions—in re-establishing the ability to support growth of mu particles, provided that the recipient cell contains at least one metagon and one or more mu particles. There is a regular lag of only one fission between introduction of such a dominant gene and its phenotypic manifestation.

7. Mathematical formulae are developed for calculating the expected initial number of metagons, the proportions of animals lacking mu particles at each fission following loss of the dominant genes, and the proportions of cells containing 0, 1, 2 …, etc. metagons per cell at any stage. The consequences of one of the possible types of irregular distribution of metagons in dividing paramecia are also considered mathematically.

Type
Research Article
Information
Genetics Research , Volume 3 , Issue 1 , February 1962 , pp. 24 - 50
Copyright
Copyright © Cambridge University Press 1962

References

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