I use E.coli on a pretty daily basis for cloning. It's alright, and there is so much work that has gone into it as a chassis organism, but overall there are definitely better organisms out there if we just took the time to figure them out (Vibrio natriegens and Bacillus subtilis are two examples).
We absolutely do not have a clear idea of how E.coli works. Hell, we don't even know how almost 1/3 of the genes work on JCVI-Syn3a works, a minimal genome we synthetically created. Far fewer in E.coli.
Ah man. Back in my university days, I worked in an infectious disease (HIV) lab that shared space with some GI docs. Went down to Mexico and came back with enteropathogenic e. coli. While they were super happy to get some fun samples and blood works, I've never felt sicker in my life.
My side would immortalize b-cells with Epstein-Barr... but that experience left me with a healthy respect for e coli.
Good point! And a related topic, we call the organism that lives happily in our gut E. coli and we also call the organisms that cause disease the same name. What’s the difference?
It turns out that the Escherichia coli (to spell out its Latin binomial) that cause disease are in some sense “diseased” themselves: the genes that enable them to be pathogenic, or make them pathogenic, I should say, are originally from a phage, a type of virus that infects bacteria [1]. In a manner that is not the same as, but conceptually similar to how HIV inserts its genes into the human’s genome, phages insert their genes (termed the “prophage”) into the bacterial genome.
In addition, most strains of pathogenic Escherichia are also holding on to an entirely separate, small, circular “genome” called a plasmid, also of exogenous origin, that contains additional genes that make them pathogenic.
So in addition to wide genome variation within the “species” (which is not really the same thing for bacteria as for mammals, mind you) of Escherichia coli, many subtypes have additional genetic material from endogenous sources that substantially changes their observed characteristics (phenotype).
koeng|1 year ago
We absolutely do not have a clear idea of how E.coli works. Hell, we don't even know how almost 1/3 of the genes work on JCVI-Syn3a works, a minimal genome we synthetically created. Far fewer in E.coli.
pazimzadeh|1 year ago
heelix|1 year ago
My side would immortalize b-cells with Epstein-Barr... but that experience left me with a healthy respect for e coli.
pazimzadeh|1 year ago
Even just within the subset of E. coli which causes UTI's, 25-40% of the genome varied between strains. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5653229/)
This diversity wasn't really appreciated in 2008 when many E. coli genomes hadn't been sequenced yet.
lysozyme|1 year ago
It turns out that the Escherichia coli (to spell out its Latin binomial) that cause disease are in some sense “diseased” themselves: the genes that enable them to be pathogenic, or make them pathogenic, I should say, are originally from a phage, a type of virus that infects bacteria [1]. In a manner that is not the same as, but conceptually similar to how HIV inserts its genes into the human’s genome, phages insert their genes (termed the “prophage”) into the bacterial genome.
In addition, most strains of pathogenic Escherichia are also holding on to an entirely separate, small, circular “genome” called a plasmid, also of exogenous origin, that contains additional genes that make them pathogenic.
So in addition to wide genome variation within the “species” (which is not really the same thing for bacteria as for mammals, mind you) of Escherichia coli, many subtypes have additional genetic material from endogenous sources that substantially changes their observed characteristics (phenotype).
1. https://en.m.wikipedia.org/wiki/Escherichia_coli_O157:H7
mncharity|1 year ago