The basic genetic toolkit to move in with your photosynthetic partner

Abstract

The origin of photosynthetic organelles via endosymbiosis more than 1 Gya ago was a major detonator of eukaryotic diversification. The evolution of a stable endosymbiotic relationship between eukaryotic cells and photosynthetic cyanobacteria involved series of cellular and molecular processes that are not entirely understood. Critical steps toward the evolution of plastids occurred when the host cell gained genetic and metabolic control over the captured cyanobacterium. Proteins recruited from the host repertoire had major roles initiating the metabolite exchange between both symbiotic partners. Concurrently, the relocation of certain cyanobacterial genes into the host nuclear genome was critical to coordinate the division of the endosymbiotic cells and the transit of nuclear-encoded proteins into the novel organelle. This review explores diverse studies that have identified key "endosymbiosis genes" and discusses the putative roles of the encoded proteins during the early evolution of plastids. The understanding of the regulation mechanisms and functions of the "endosymbiosis genes" will shed light on the design of genetic engineering approaches to facilitate endosymbiotic associations.

The economics of organellar gene loss and endosymbiotic gene transfer

“…For example, it has been proposed that it protects endosymbiont genes from mutational hazard (Allen and Raven 1996; Lynch, et al 2006; Smith 2016; Speijer, et al 2020), and that it enables endosymbiont genes that are otherwise trapped in a haploid genome to recombine and thus escape from Muller’s ratchet (Muller 1964; Lynch 1996; Martin and Herrmann 1998; Lynch, et al 2006; Neiman and Taylor 2009; Smith 2016). It has also been proposed that endosymbiotic gene transfer is an inevitable consequence of a constant stream of endosymbiont genes entering the nucleus (Doolittle 1998), and that transfer to the nuclear genome allows the host cell to gain better control over the replication and function of the organelle (Herrmann 1997) allowing better cellular network integration (Nowack, et al 2010; Reyes-Prieto 2015). However, mutation rates of organellar genes are often not higher than nuclear genes (Wolfe, et al 1987; Lynch, et al 2006; Lynch, et al 2007; Drouin, et al 2008; Smith 2015; Smith and Keeling 2015; Smith 2016; Grisdale, et al 2019) and therefore effective mechanisms for protection against DNA damage in organelles must exist.…”