Dynamic genomic architecture of mutualistic cooperation in a wild population of Mesorhizobium

Research on mutualism seeks to explain how cooperation can be maintained when uncooperative mutants co-occur with cooperative kin. Gains and losses of the gene modules required for cooperation punctuate symbiont phylogenies and drive lifestyle transitions between cooperative symbionts and uncooperative free-living lineages over evolutionary time. Yet whether uncooperative symbionts commonly evolve from within cooperative symbiont populations or from within distantly related lineages with antagonistic or free-living lifestyles (i.e., third-party mutualism exploiters or parasites), remains controversial. We use genomic data to show that genotypes that differ in the presence or absence of large islands of symbiosis genes are common within a single wild recombining population of Mesorhizobium symbionts isolated from host tissues and are an important source of standing heritable variation in cooperation in this population. In a focal population of Mesorhizobium , uncooperative variants that lack a symbiosis island segregate at 16% frequency in nodules, and genome size and symbiosis gene number are positively correlated with cooperation. This finding contrasts with the genomic architecture of variation in cooperation in other symbiont populations isolated from host tissues in which the islands of genes underlying cooperation are ubiquitous and variation in cooperation is primarily driven by allelic substitution and individual gene gain and loss events. Our study demonstrates that uncooperative mutants within mutualist populations can comprise a significant component of genetic variation in nature, providing biological rationale for models and experiments that seek to explain the maintenance of mutualism in the face of non-cooperators

Mitochondria Inspire a Lifestyle

Tucked inside our cells, we animals (and plants, and fungi) carry mitochondria, minuscule descendants of bacteria that invaded our common ancestor 2 billion years ago. This unplanned breakthrough endowed our ancestors with a convenient, portable source of energy, enabling them to progress towards more ambitious forms of life. Mitochondria still manufacture most of our energy; we have evolved to invest it to grow and produce offspring, and to last long enough to make it all happen. Yet because the continuous generation of energy is inevitably linked to that of toxic free radicals, mitochondria give us life and give us death. Stripping away clutter and minutiae, here we present a big-picture perspective of how mitochondria work, how they are passed on virtually only by mothers, and how they shape the lifestyles of species and individuals. We discuss why restricting food prolongs lifespan, why reproducing shortens it, and why moving about protects us from free radicals despite increasing their production. We show that our immune cells use special mitochondria to keep control over our gut microbes. And we lay out how the fabrication of energy and free radicals sets the internal clocks that command our everyday rhythms-waking, eating, sleeping. Mitochondria run the show