General acclimation responses co-opted for somatic cell differentiation in Volvox carteri
Aurora M. Nedelcu
Department of Biology, University of New Brunswick, Fredericton, New Brunswick, Canada E3B 5A3
The evolution of a sterile soma was instrumental to the increase in complexity in many multicellular lineages. We have previously proposed that the evolution of soma in the green alga, Volvox carteri, involved the co-option of a life-history gene whose expression in its Chlamydomonas-like unicellular ancestor was conditioned on an environmental cue (as an adaptive strategy to enhance survival at an immediate cost to reproduction), through shifting its expression from a temporal (environmentally-induced) into a spatial (developmental) context. To test this hypothesis, we investigated the expression of rls1 - which is the closest Chlamydomonas reinhardtii homolog of the gene responsible for the permanent suppression of reproduction in the somatic cells of V. carteri. Here, we report that rls1 is expressed under multiple stress conditions (phosphorus-, sulfur- and light-deprivation; stationary phase) and its induction coincides with a decline in reproduction potential. Overall, these findings suggest that rls1 is part of the general acclimation response (which entails various photosynthetic and metabolic changes that ultimately result in the temporary cessation of cell growth and division) and, because it codes for a putative transcription factor, might function as a regulator of acclimation in C. reinhardtii. In support of this suggestion is the fact that an inhibitor of the photosynthetic electron flow that triggers acclimation-like responses also induces rls1 expression. Based on these findings we propose a model for the evolution of soma, in which by simulating an acclimation signal (i.e., a change in cellular redox status) in a developmental rather than environmental context, responses beneficial to a unicellular individual can be co-opted into cell differentiation in a multicellular context. The model also provides a mechanism that can translate differences in embryonic cell size (often associated with cell differentiation) into differences in gene expression.
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