· That you can prime for what’s coming with “the first challenges for an endosymbiont are to avoid being digested by the host“ although that conflates the origin of the eukaryotic cell with the origin of e.g. the plastid in a eukaryotic cell.
· That mitochondria and plastid endosymbiosis was somehow the same process, only the involved pathogens were different.
· That Loki did endocytosis first, not phagocytosis, and that it has nothing to do with the acquisition of the mitochondrion because that was infection or maybe not – depends a bit on what paragraph you read.
· That the mito was a Rickettsia, like those living today.
· That you can use Spang et al. 2015 as a citation for: “The latter would have allowed the capture of the mitochondrial precursor.”
· That Gomes and Dikic 2014 write about an archaeal host that “evolved mechanisms such as autophagy, production of antimicrobial peptides, and reactive oxygen species induction to protect itself“, although they don't.
· That Lane and Martin 2010 provide support that all that mitos did for the host was to allow it to evolve endocytosis into phagocytosis.
· That Rickettsia are among the very few pathogens that can multiply directly in the host cytosol outside of an inclusion vesicle (or is it parasitophorous vacuole?) and that there’s no need to even mention Shigella, Listeria, Burkholderia or Francisella (see e.g. Ray et al. 2009 Nat Rev Microbiol).
· That the endosymbiont was not a symbiont, but a pathogen and needed to evade the immune system. (But what if they were epibionts before and hence symbionts?). Syntrophy among prokaryotes is the norm, infection of one prokaryote by another everything but that.
· That Loki (that still no one has seen and hence studied) has a kind of immune system, because it messed up endocytosis.
· That Loki likely invented autophagy to remove the “incidental capture of harmful bacteria” that entered Loki by mistake (at no energetic cost) due to ongoing endocytosis. Imagine going for a steak (peptide) and evidently incorporating a whole cow (proteobacterium).
· That, hence, endocytosis is apparently not receptor-mediated and the different machineries used do not matter too much and we can throw everything into one pot without explaining.
· That endocytosis in archaea evolved for the purpose of scavenging substrate, in an unselected manner, from the environment.
· That you can write: “The discovery of the Lokiarchaeota thus provides a potential missing link in the story of eukaryote evolution: membrane trafficking, mitochondrion-lacking cells that could have hosted the mitochondrial endosymbiosis.“ right next to and on the very same page: “These results also help explain why ancestrally mitochondrion-lacking eukaryotes (so-called archezoans) have never been found: They likely do not exist.“ A phagocytosing archeaon (and hence one with the need of eukaryotic complexity) but no mito is an Archezoan.
· That you need no lysosome, no MVBs, no ER, no Golgi and no vacuole to process endosomes and that you can do so while citing papers that write: “According to the current view, the phagophore originates from endoplasmic reticulum and mitochondrial membranes, in particular, mitochondria-associated endoplasmic reticulum membranes (MAMs). Further expansion of the nascent autophagosome seems to occur by fusion with membranes from different sources, including Golgi, plasma membrane, and recycling endosomes“.
· That the fact that the plasma membrane of archaea is a bioenergetic one poses no problem when inventing endocytosis.
· That single-cells can flush their cytosol with ROS at no cost.
· That it might be time we change the word endosymbiosis to endopathogeneiosis.
· That you can ignore several papers by several labs that do not pick up Chlamydiae above background noise. I'd say that view don't matter as much as balance does.
· That it takes creationists only days to use this article as evidence that “evolutionists” don’t understand endosymbiosis (http://crev.info/2016/02/how-well-do-evolutionists-understand-endosymbiosis/).