endosymbiosis.
13 of 1538 NOTE documents. Back to the full index.
| # | Title | Summary | Status |
|---|---|---|---|
| NOTE-1211 | Athreya, Czuppon & Gokhale — The evolution of dependence and cohesion in incipient endosymbioses | An adaptive-dynamics model in which hosts, symbionts and host–symbiont collectives are three populations. Each partner has an “obligacy” (investment in collective rather than free-living growth) and an “adhesion” (investment in synchronized, collective reproduction). The faster-growing partner, the symbiont, becomes fully obligate first. What the host’s obligacy then does depends on within-collective births and deaths: it stays, rises to full dependence, or falls to none. Obligacy rises only if the collective’s carrying capacity is high enough; collective growth rate does not matter. Early on, dependence evolves ahead of cohesion. That last result holds for the trait mapping the authors chose, and their own Table S1 reverses it under the opposite mapping. The authors say the available data can neither confirm nor refute it. | Read |
| NOTE-1212 | Morris, Lenski & Zinser — The Black Queen Hypothesis | Proposes that in free-living microbes, losing a costly function whose product leaks to neighbours is favoured by ordinary individual selection, and the loss runs until the remaining producers (“helpers”) just supply the community, leaving most cells (“beneficiaries”) dependent on a rare few. No relatedness, cooperation or collective is needed, only leakiness and frequency dependence. The one worked case is the loss of catalase-peroxidase (katG) in Prochlorococcus, which cannot survive the hydrogen peroxide that its community removes. The other cases are suggestions. | Read |
| NOTE-1213 | McCutcheon, Garber, Spencer & Warren — How do bacterial endosymbionts work with so few genes? | An essay on the endosymbionts with genomes under about 200 kb, which the authors call “tipping-point endosymbionts”. Below about 400 kb, symbionts almost always lose the genes to build their own envelope and to move proteins across it. Below about 200 kb, even translation erodes: ribosomal proteins, tRNAs and aminoacyl-tRNA synthetases go. Their proteomes are among the most compositionally biased in bacteria. The paper asks four questions it cannot answer: where their membranes, transporters, missing translation parts and protein stability come from. Its best guess is from the host, as in organelles. The thresholds come from a hand-picked set of genomes, and the composition analysis is called preliminary. | Read |
| NOTE-1234 | Kay et al. — Dated gene duplications and the assembly of eukaryotes | A relaxed molecular clock dates 135 gene duplications that happened on the two stem lineages of eukaryotes, inside a species tree dated with 18 fossil calibrations. The authors take the onset of duplications in genes of alphaproteobacterial origin, about 2.2 billion years ago, as the mark of mitochondrial endosymbiosis. Most duplications of archaeal origin are older than that, including ones in actin, tubulin, vesicle trafficking and nuclear-targeted families, so the host was already elaborating its cytoskeleton, endomembranes and nuclear machinery. Most duplications of non-alphaproteobacterial bacterial genes come later, which the authors take as evidence against serial endosymbiosis. Each duplication date is a maximum age for its paralogues’ functions, many intervals reach below 2.2 billion years, and the order of phagocytosis and the mitochondrion is left open by the authors. | Read |
| NOTE-1235 | Campbell et al. — Changes in endosymbiont complexity drive host-level compensatory adaptations in cicadas | In cicadas whose endosymbiont Hodgkinia has split into many lineages, each essential, the mother must put every lineage into every egg. A simulation shows that random transmission would need far more cells as lineages multiply and grow uneven. Counts in eggs of four species find Sulcia numbers roughly constant, and Hodgkinia numbers up to about six times higher in Magicicada septendecim than in a single-lineage species. Amplicon sequencing found every tracked Hodgkinia genotype in every egg sampled. The transmission route looks the same under the light microscope. Only M. septendecim differs significantly; the six-lineage species does not. So the compensation rests on one species. The authors call the raised titre a cost of fragmentation, and speculate that it could feed further splitting. | Read |
| NOTE-1236 | Shigenobu, Watanabe, Hattori, Sakaki & Ishikawa — Genome sequence of the endocellular bacterial symbiont of aphids Buchnera sp. APS | The first complete genome of an obligate insect endosymbiont. Buchnera APS, from the pea aphid, has a 640,681-bp chromosome with 583 ORFs and two small plasmids. It is a subset of the E. coli gene set, produced by loss from a larger common ancestor. It keeps the pathways for the amino acids its host cannot make, lacks almost all of those the host can, and draws some precursors from the host, so the two partners’ pathways interlock. It also lacks phospholipid and lipopolysaccharide synthesis, almost all transcriptional regulators, and recA and uvrABC. The authors infer that it can live only in the bacteriocyte and compare it to an organelle. Everything here is read from gene content; no experiment on the symbiont is reported, and the host’s dependence is asserted from the literature, not shown. | Read |
| NOTE-1237 | Bernabeu, Manzano-Morales, Marcet-Houben & Gabaldón — Gene ancestries reveal diverse microbial associations during eukaryogenesis | A fresh reconstruction of the last eukaryotic common ancestor’s proteome from three 100-genome eukaryotic datasets, with each family’s origin read from its sister group in a maximum-likelihood tree. Under thresholds tuned to maximize assignments to Alphaproteobacteria and Asgard archaea, two further bacterial donors pass in every dataset, Myxococcota (3.92% of the proteome) and Planctomycetota (2.24%), comparable to Alphaproteobacteria (3.99%) and Asgard (3.28%). A control that removes Alphaproteobacteria from the database does not reproduce their pattern. About 4.5% of families have a viral sister, mostly giant viruses. Stem-length distributions place Asgard earliest and Planctomycetota before the mitochondrion and Myxococcota. The authors read this as waves of transfer from several partners and challenge two-partner models. They concede their data say nothing about whether any donor was a symbiont. | Read |
| NOTE-1238 | Imachi et al. — Isolation of an Asgard archaeon at the prokaryote–eukaryote interface | After 12 years from sampling to culture, an archaeon of the Asgard group, Ca. Prometheoarchaeum syntrophicum MK-D1, was obtained in stable co-culture with a methanogen (not alone, hence the Candidatus name). It is a small coccus, about 550 nm across, doubling in 14–25 days. It degrades amino acids only in syntrophy, handing off hydrogen and formate to partners that can be swapped. It has long, often branching membrane protrusions and no visible internal compartments. It is the closest cultured relative of eukaryotes, among cultured organisms only. From its genome and other Asgard genomes the authors propose that the Asgard ancestor was a partner-dependent amino-acid degrader. The entangle–engulf–endogenize model they build on it is a hypothesis that the authors call not definitive. | Read |
| NOTE-1239 | Santana-Molina, Williams, Snel & Spang — Chimeric origins and dynamic evolution of central carbon metabolism in eukaryotes | Sixty-four gene-family phylogenies for eukaryotic central carbon metabolism (glycolysis, the pentose phosphate pathway, pyruvate and acetate conversion, and the TCA cycle), set against a 317-marker eukaryotic species tree. LECA had essentially the whole pathway set. Its enzymes came from several sources: six putative Asgard contributions, mostly cytosolic glycolytic and pentose-phosphate enzymes (support between 39% and 97%, two cases ambiguous); seventeen alphaproteobacterial ones, mostly mitochondrial and ten of them in the TCA cycle; and others from various bacteria, with no third dominant donor. Since then, loss, horizontal replacement and retargeting have reshaped the pathways, and targeting no longer follows origin. The authors read the split, archaeal glycolysis in the cytosol and bacterial TCA in the mitochondrion, as support for syntrophy models. The split is what any archaeal-host, bacterial-endosymbiont model predicts, so it does not single syntrophy out. | Read |
| NOTE-1240 | Pittis & Gabaldón — Late acquisition of mitochondria by a chimaeric host | For 1,078 eukaryotic protein families inferred to be present in LECA, the length of the branch joining each family to its closest prokaryotic relatives, divided by the family’s median branch length within eukaryotes, is shortest for families of alphaproteobacterial origin and mitochondrial location, longer for other bacterial families (endomembrane-associated), and longest for archaeal families (nucleus and information processing). Read as time, that puts the mitochondrion last, into a host whose proteome was already chimaeric. The reading of length as time needs rates before and after LECA to be proportional, the alphaproteobacterial difference from other bacteria is marginal (P = 0.044), and stem length also falls when a closer relative is sampled, as the paper’s own Lokiarchaeota control shows. | Read |
| NOTE-1241 | Sørensen, Stiller, Kröninger & Nowack — Protein import into bacterial endosymbionts and evolving organelles | A review of the evidence that hosts import their own proteins into bacterial endosymbionts, which has long been taken to mark an organelle off from an endosymbiont. Import of hundreds of nucleus-encoded proteins is established, by proteomics of isolated endosymbionts, in two systems only: the chromatophore of Paulinella and the nitroplast of Braarudosphaera. In both, the imported proteins come mostly from the host’s own genes and from bacteria other than the endosymbiont, and the authors say that gene transfer from the endosymbiont “is not a precondition” for genetic integration. Elsewhere, in a trypanosomatid, a diatom and four insects, there are one to seven imported or targeted proteins per system, each found by antibodies or proteomics. The authors propose an order, effector proteins first and dependence on an imported redundant protein second, which they call plausible on limited data. The import mechanisms are almost entirely unknown. | Read |
| NOTE-1242 | Tobiasson, Luo, Wolf & Koonin — Dominant contribution of Asgard archaea to eukaryogenesis | A large phylogenomic survey that assigns each widespread eukaryotic protein family to its most likely prokaryotic sister by likelihood weights on constrained trees. In the 4,290 best-resolved families, Asgard archaea take about half of all likelihood weight and lead in nearly every functional system, information processing above all. Alphaproteobacteria contribute a small, coherent set centred on the mitochondrion (oxidative phosphorylation, Fe–S cluster assembly, mitochondrial translation). About a third of families point to other bacteria, scattered across functions with no pathway from one donor except a narrow Myxococcota signal, which the authors read as piecemeal gene transfer and not further symbioses. A stem-length analysis leads them to doubt that stem lengths time gene acquisition. They favour a complex Asgard ancestor that took up the mitochondrion late. The limiting caveat, theirs, is sparse and biased genome sampling. | Read |
| NOTE-1243 | Karnkowska et al. — The oxymonad genome displays canonical eukaryotic complexity without a mitochondrion | An inventory of the draft genome of Monocercomonoides exilis, an oxymonad gut commensal and the only well-studied eukaryote with no mitochondrion. Apart from the mitochondrion, peroxisomes and the machinery for degrading them, nothing in the cell looks reduced: about 75 Mb, 16,768 genes, 31,693 introns, and canonical systems for DNA replication and repair, transcription, the cytoskeleton, membrane trafficking and autophagy. It has kept more ancestral eukaryotic protein families than the parasitic metamonads. The only changes the authors tie to the loss are two preadaptations, the SUF system for Fe–S clusters, which all examined relatives share, and the loss of the glycine cleavage system and SHMT, plus the loss of mitophagy. No gene was found that compensates for the absence. The work is homology searches on a draft genome, with two cells imaged by FIB-SEM. | Read |