Symbiosis, as we all know, is that lovely relationship where two organisms mutually benefit from a dependent relationship. Aphids, for example, feed entirely on plant phloem, which is lacking certain amino acids. Their bacterial symbiont synthesizes these amino acids, while getting other necessary nutrients from the aphids. The bacterial genome shows the signs of this remarkable relationship, having a much reduced size with only certain necessary genes.

But the fact that the aphids and bacteria both need each other to reproduce means that mutations in the bacteria may have a phenotype in the aphid, and vice versa. This has been elegantly demonstrated in a new paper, Aphid thermal tolerance is governed by a point mutation in bacterial symbionts. The title pretty much says it all, but I'll quote a bit from the abstract:

A model of obligate symbiosis is that between aphids and the bacterium Buchnera aphidicola, which supplies essential nutrients. We report a mutation in Buchnera of the aphid Acyrthosiphon pisum that recurs in laboratory lines and occurs in field populations. This single nucleotide deletion affects a homopolymeric run within the heat-shock transcriptional promoter for ibpA, encoding a small heat-shock protein. This Buchnera mutation virtually eliminates the transcriptional response of ibpA to heat stress and lowers its expression even at cool or moderate temperatures. Furthermore, this symbiont mutation dramatically affects host fitness in a manner dependent on thermal environment. Following a short heat exposure as juveniles, aphids bearing short-allele symbionts produced few or no progeny and contained almost no Buchnera, in contrast to aphids bearing symbionts without the deletion. Conversely, under constant cool conditions, aphids containing symbionts with the short allele reproduced earlier and maintained higher reproductive rates.

Humans, of course, are superorganisms, in that we're infested with billions and billions of microorganisms. We could reproduce without them, I imagine (though it would be pretty tough to test that hypothesis), but there's much evidence that the genotypes of out residents plays a role in all manners of phenotype. In this aphid case, ths role is particularly striking-- do aphids have one genome, or two? Perhaps it's best to think of this as a mitochondrial DNA-like mutation.