Organelle genes – do they jump or are they pushed?

• Published in: Trends in genetics 2000-02, Vol.16 (2), p.65-66
• Main Authors: Howe, Christopher J., Barbrook, Adrian C., Lockhart, Peter J.
• Format: Article
• Language: English
• Subjects: Animals; DNA Damage; DNA, Mitochondrial - genetics; Eukaryota - genetics; Gene transposition; Genome; Loss of organelle genes to nuclear genome; Organelle genome; Organelles - genetics; Plastid genome; Plastids - genetics; Reclinomonas americana
• ISSN: 0168-9525
• DOI: 10.1016/S0168-9525(99)01919-8

Race et al. presented a stimulating account of the likely reason for retention of genes in some organelles in September's issue. As they made clear, this begs the question of what drives the loss of genes to the nucleus anyway. They described suggestions that the selection pressure might arise from Muller's ratchet, exacerbated by the occurrence of DNA-damaging processes in the organelles. We would like to suggest another explanation (that might act together with Muller's ratchet), based on our studies of plastid genomes. These genomes have a tendency to become AT rich, both in coding and in non-coding regions. The reason for this is unknown, but it might be a consequence of the nature of the DNA damage to which the genomes are exposed. The high AT content affects the amino acid composition of the encoded proteins. Plastid genes are enriched in codons for Phe, Ile, Lys, Asn and Tyr and depleted in codons for Ala, Gly and Pro by comparison with genes for the same proteins from the nucleus or prokaryotes. For some proteins, this shift in their amino acid composition might be sufficiently deleterious to their function to provide a significant selective advantage for their transposition to the nucleus. Mitochondrial genomes are also AT rich, so the same processes might operate there. Therefore, transposed genes can be seen as 'molecular refugees' fleeing from an oppressive genomic environment that is trying to force them into encoding unsuitable proteins. Their freedom of movement might be limited by other factors, perhaps including membrane integrity, allowing some very AT-rich genomes (such as the mitochondrial genome of Reclinomonas americana) to retain a larger genetic complement than usual.