Sexual reproduction and parent-offspring conflict in the RNA “Tumour” virus/host relationship: Implications for vertebrate oncogene evolution

Abstract

The following aspects of RNA tumour virus biology are stressed: (a) their relationship to transformation, i.e. their presence may cause transformation almost immediately, influence it probabalistically, be associated or not associated with transformation; (b) transmission may be horizontal or vertical (genetic or congenital); (c) viral interaction may lead to interference or genotypic or phenotypic mixing. The oncogene and protovirus hypotheses are discussed. Bearing the above in mind the following suggestions are made. (A) virus/host interaction (a) Those RNA viruses able to induce almost immediate transformation are pathogens. (b) Other types may perhaps be regarded as host genes able to alternate between the integrated and autonomous states. (c) Host alleles controlling these latter viruses have the characteristics of a complex mating control system, influencing the entry (and therefore recombination and conversion into the autonomous state) of certain groups of genes. Such recombination may sometimes be interspecific. (B) oncogene expression (a) Age and sex dependent oncogene expression occurs in periods of low “host” viability i.e. when transformation has a small effect on “host” fitness. (b) These periods are associated with immune system defects. (C) oncogene evolution Considerations in the evolution of a vertebrate oncogene may include:— (a) Transformation may be controlled by an altruistic “death allele”, active in young offspring of low viability, this allele saves parental care. (b) Genetically modified cells may be regarded as sexually reproduced progeny. Somatic and germ cell offspring are selected to extract the maximum possible parental investment. The reproductive success obtained from parental care is devalued by the effect on relatives (CR) and their degree of relatedness (Ro). New genetic material and low parent fitness reduces Ro and CR respectively. Any agent (chemicals, radiation or viruses) which reduces Ro or CR may be oncogenic without carrying oncogenes . (c) Transformation may increase the probability of horizontal transmission of that cells genotype and may be regarded as requiring parental investment. (d) Parent/offspring conflict (in the division of investment) predicts that the parent cells will “disagree” with the offspring cell as to when transformation should occur. (e) The oncogene is a vertebrate gene, the preceding points closely resemble the protovirus hypothesis except that conditions for gene expression (and not the gene itself) arise anew by recombination, mutation and ageing in each new generation.