Vertebrate hearts have at least two chambers. But how did these evolve from the single-chambered pumps seen in simpler organisms? While examining the development of the heart of the sea squirt, Brad Davidson and colleagues (Genes Dev. 20, 2728–2738; 2006) may have chanced on the answer.

The adult sea squirt (Ciona intestinalis, pictured) is a classic squishy invertebrate, but as a larval tadpole it resembles a fish embryo. This puts it closer to humans on the evolutionary scale than other genetic model organisms such as fruitflies and worms, and makes it a useful system for studying certain developmental processes.

Davidson et al. followed the single-chambered sea-squirt heart as it grew from two cells in the early embryo. These cells divide and specialize to form muscle cells in either the heart or the tadpole tail. The authors find that the decision about which muscle type develops centres on a gene-regulatory factor called Ets1/2 — cells in which the factor is active become heart cells.

Credit: K. TELNES/IMAGE QUEST MARINE

But Ets1/2 is also present, though inactive, in the cells destined to become tail. So something must activate it to set embryonic cells on the path to becoming heart cells. Davidson et al. teased apart the genetics to discover that the activating signal comes from a classic growth factor called FGF. Both Ets1/2 and the FGF signalling pathway have relatives in vertebrates, and these have been linked to heart development. This implies that the developmental pathway in the sea squirt has been conserved through evolution.

The twist in the tale came from an experiment in which Davidson and colleagues looked at the effect of a permanently active form of Ets1/2 on embryonic cells destined to become tail. Not only did these cells develop into heart cells, confirming the role of Ets1/2, but in some animals the resulting organ had two chambers rather than one.

So the authors speculate that since it separated from the sea-squirt lineage, an ancestral vertebrate recruited additional heart precursor cells to make a two-chambered heart. As their study shows, even a subtle change in signalling in the pool of cells that can form muscle cells might have allowed this transition.