nucleation

QUESTION-277: When formerly autonomous partners come to depend on one another, which of mutual dependence, reproductive cohesion, the distribution of essential functions across genomes, the host's regulatory control and the alignment of selection does each route to dependence bring about, and which of them, alone or together, make the partnership a new evolutionary individual?

12 min read

Properties7
StatusOpen
Version5
Tagsindividuation, philosophy-of-biology, endosymbiosis
Linedistributed-agency
RefinesQUESTION-035 — Relative to a stated target, when is a combined form one system, where does its boundary lie, and how long does it last?
Cited as “bears on” byCLAIM-506 — The split of the last eukaryotic common ancestor's central carbon metabolism, archaeal enzymes in the cytosol and alphaproteobacterial ones in the mitochondrion, does not single out syntrophy: a host that kept its own archaeal glycolysis and took up a bacterium with a TCA cycle leaves it whether the partnership began in syntrophy or by engulfment by an already complex host, and what the split counts against is a host whose carbon metabolism was replaced by the symbiont's, CLAIM-508 — Gene ancestries alone cannot tell a symbiotic partner from a source of transferred genes: a partner whose genes were mostly lost, replaced or spread thin would leave the diffuse trace that Tobiasson and colleagues read as piecemeal transfer, and Bernabeu and colleagues concede that their donor signals say nothing of the kind of interaction, CLAIM-509 — Stem lengths alone do not establish an order of acquisition in eukaryogenesis, neither Pittis and Gabaldón's late mitochondrion nor Bernabeu and colleagues' transfer waves: normalized stem length measures time only if rates before and after LECA are proportional, it shortens as closer relatives are sampled, the alphaproteobacterial separation from other bacteria rests on P = 0.044, and on Tobiasson and colleagues' data it does not behave as a clock, THEORY-1048 — On the Black Queen Hypothesis of Morris, Lenski and Zinser, losing a costly function whose product leaks to neighbours is favoured by ordinary individual selection in large free-living microbial populations, and the loss proceeds until the remaining producers just supply the community, so that most cells come to depend on a rare few with no relatedness, cooperation or collective required, THEORY-1049 — On McCutcheon and colleagues' survey, bacterial endosymbionts lose their own cell-envelope and envelope-transport genes together below about 400 kb, and begin to lose translation genes (ribosomal proteins, tRNAs, aminoacyl-tRNA synthetases) below about 200 kb, so that the smallest-genome symbionts cannot be self-sufficient and their membranes, transport and protein synthesis are presumably supplied by the host, as for organelles, THEORY-1050 — In Athreya, Czuppon and Gokhale's adaptive-dynamics model of an incipient endosymbiosis, mutual dependence (the product of the partners' obligacies) evolves ahead of reproductive cohesion (the product of their adhesions) early on, but only under the mapping in which each partner's free-living growth depends on its own obligacy alone while dissociation depends on both partners' adhesions; the authors' own appendix shows the bias vanishing under matched mappings and reversing under the opposite one, and their survey of real symbioses cannot test it, THEORY-1051 — In Athreya, Czuppon and Gokhale's model of an incipient endosymbiosis, the partner with the larger and faster-growing population evolves faster and becomes fully obligate first, which the authors read as a Red King effect in which the collective's shared fate aligns interests; with equal within-collective rates for both partners, the other partner's dependence then stays where it was, rises to full dependence, or falls to none, according to whether partners are born or die inside the collective; and in its simulations dependence rose from zero at the higher collective carrying capacities tried and not at the lowest, under a condition the authors show sufficient and not necessary, so a full transition to a mutually dependent, co-reproducing pair is a parameter-dependent outcome and not the default, THEORY-1098 — On Karnkowska and colleagues' genome analysis, the oxymonad Monocercomonoides exilis lost its mitochondrion only after the organelle's essential functions had been removed one by one, Fe–S cluster assembly to a bacterial-type SUF system shared with mitochondriate relatives and then the glycine cleavage system by loss, and the loss left the rest of the cell canonical, with no compensating changes found, THEORY-1099 — On Kay and colleagues' relaxed-clock dating of pre-LECA gene duplications, most duplications in eukaryotic gene families of archaeal origin, including actin, tubulin, vesicle-trafficking and nuclear-targeted families, predate the onset of duplications in genes of alphaproteobacterial origin at about 2.2 billion years ago, which the authors take as the start of mitochondrial endosymbiosis, so the host was elaborating its cytoskeleton, endomembranes and nuclear machinery before the mitochondrion; each 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, THEORY-1100 — On Sørensen and colleagues' review, a bacterial endosymbiont becomes genetically integrated, the authors' mark of an organelle, when nuclear genes whose products are imported into it functionally replace essential genes it has lost, and this does not require gene transfer from the endosymbiont: in the Paulinella chromatophore and the nitroplast, the two systems with hundreds of imported proteins, many of which fill gaps left by lost genes, the imported proteins come mostly from the host's own genes or from other bacteria, and in the nitroplast no gene transfer from the endosymbiont has been found, THEORY-1101 — Tobiasson, Luo, Wolf and Koonin find, on 5,850 eukaryotic gene stems, that normalized stem length does not behave as a clock of acquisition time: alphaproteobacterial stems are longer than Asgard ones for the 70% of stems below 0.3 and shorter only above 0.35, oxidative-phosphorylation genes presumed acquired together vary by more than two orders of magnitude, and information-processing genes have short stems; they conclude that even normalized stem lengths are set primarily by factors other than acquisition time, at least over the long timescales analysed, and suggest that adaptation after acquisition lengthens stems, THEORY-1102 — On Pittis and Gabaldón's stem-length analysis of the LECA proteome, families of alphaproteobacterial origin and mitochondrial location sit closer to their prokaryotic relatives, after correction for each family's rate, than families of other bacterial origin (P = 0.044), which sit closer than archaeal families, and the authors read this as late acquisition of the mitochondrion by a host whose proteome was already chimaeric, under their stated assumption that rates before and after LECA are correlated, THEORY-1103 — On Shigenobu and colleagues' genome of Buchnera sp. APS, the aphid symbiont keeps the genes for the amino acids its host cannot make and has lost almost all of those its host can, uses host-made glutamate and aspartate as precursors, and lacks phospholipid synthesis and nearly all its own transcriptional regulators, so that its metabolism interlocks with the host's and it presumably lives only inside the bacteriocyte, a state reached by gene loss from an E. coli-like ancestor, THEORY-1104 — In Tobiasson, Luo, Wolf and Koonin's constrained-tree survey of widespread eukaryotic protein families, Asgard archaea are the largest single prokaryotic source, with about half the likelihood weight in the best-resolved families and the lead in nearly every functional system, while Alphaproteobacteria contribute a small, coherent set centred on the mitochondrion and other bacteria about a third of families, scattered across functions with no pathway led by one donor except a narrow Myxococcota signal in nucleotide-sugar and nicotinate metabolism; the authors read this as one Asgard host lineage, one endosymbiont and piecemeal gene transfer rather than further symbioses, THEORY-1105 — In Bernabeu, Manzano-Morales, Marcet-Houben and Gabaldón's reconstruction of the last eukaryotic common ancestor's proteome, two bacterial phyla besides the mitochondrial ancestor, Myxococcota and Planctomycetota, each account for a share of the proteome comparable to that of Alphaproteobacteria and Asgard archaea under thresholds calibrated on those accepted partners, and stem-length distributions order the acquisitions as waves, Asgard first, then Planctomycetota, then the mitochondrial ancestor and Myxococcota together; the authors read this as serial associations with several partners, while conceding that their data cannot say whether any donor was a symbiont, THEORY-1106 — Campbell and colleagues report, from four cicada species with five or six eggs each, that Hodgkinia cells per egg range from about 4,900 in a species with one Hodgkinia lineage to about 30,000, some six times as many, in Magicicada septendecim, whose Hodgkinia has split into many interdependent lineages and the only species that differs significantly, while Sulcia numbers are not raised, the transmission route is the same, and every egg sampled carries every lineage tracked by marker genes; the authors take the raised titre as a host adaptation that compensates for the symbiont's fragmentation, and a cost of it, THEORY-1107 — On Sørensen and colleagues' scenario, an endosymbiont becomes an organelle in steps: the host first targets effector proteins into it; an imported host protein redundant with one of its functions then lets the endosymbiont's own gene decay, making it dependent; and a general import pathway, once evolved, brings in hundreds of proteins; this genetic integration arises only in permanent, vertically transmitted associations, and host effector control without vertical transmission, as in rhizobia, does not lead to it, THEORY-1108 — On Imachi and colleagues' cultivation of Candidatus Prometheoarchaeum syntrophicum MK-D1, the first Asgard archaeon grown in the laboratory is a small, internally simple coccus with long branching protrusions that degrades amino acids only in syntrophy, handing hydrogen and formate to partners that can be exchanged, and from its genome and other Asgard genomes the authors infer that the Asgard ancestor was likewise dependent on metabolic partners; the isolate is a modern relative separated from the host lineage by about two billion years, grown only in co-culture, and the entangle–engulf–endogenize model built on it is a hypothesis the authors call not definitive, THEORY-1109 — Santana-Molina, Williams, Snel and Spang find that the last eukaryotic common ancestor's central carbon metabolism was chimeric: a few Asgard-archaeal enzymes in cytosolic glycolysis and the pentose phosphate pathway, four placed with Asgard archaea at bootstrap 39–97% and two ambiguously, most alphaproteobacterial ones in the mitochondrial TCA cycle and pyruvate conversion, and others from various bacteria with no third dominant donor, since remodelled by loss, horizontal replacement and retargeting so that compartment no longer follows origin; the authors take the cytosol–mitochondrion split as support for syntrophy, THEORY-1197 — Eukaryogenesis involved one archaeal host lineage, of Asgard descent, and one bacterial endosymbiont, the alphaproteobacterial ancestor of mitochondria; the eukaryotic genes from other bacteria came by piecemeal gene transfer, not from further symbiotic partners, THEORY-1200 — The Asgard archaeal ancestor of eukaryotes depended on metabolic partners: like Candidatus Prometheoarchaeum syntrophicum, it degraded amino acids in syntrophy, handing hydrogen and formate to partners that removed them, THEORY-1201 — Normalized stem length is not a clock of gene acquisition time: it is set mainly by factors other than when a gene was acquired, such as adaptation to the new cell after acquisition, so relative timings of eukaryogenesis drawn from stem lengths alone are not supported, THEORY-1203 — The host lineage elaborated its cytoskeleton, endomembrane system and nuclear machinery before mitochondrial endosymbiosis began, about 2.2 billion years ago: most pre-LECA duplications in eukaryotic gene families of archaeal origin predate it, THEORY-1205 — Eukaryotes began in a syntrophic partnership: an archaeal host fermented sugars and passed reducing equivalents to an alphaproteobacterial endosymbiont that contributed a TCA cycle and an electron transport chain, which is why the last eukaryotic common ancestor's central carbon metabolism is archaeal in cytosolic glycolysis and the pentose phosphate pathway and alphaproteobacterial in the mitochondrial TCA cycle, THEORY-1206 — The mitochondrion was acquired late in eukaryogenesis, by a host whose proteome was already chimaeric, with genes from several bacterial sources acquired before it, THEORY-1208 — Bacterial endosymbionts lose their cell-envelope and envelope-transport genes together below about 400 kb and begin to lose translation genes below about 200 kb, and the host supplies the membranes, transport and protein synthesis that the smallest-genome symbionts no longer encode, as for organelles, THEORY-1211 — An endosymbiont becomes an organelle in steps: the host first targets effector proteins into it; an imported host protein redundant with one of its functions then lets the endosymbiont's own gene decay, making it dependent; and a general import pathway, once evolved, brings in hundreds of proteins; this genetic integration arises only in permanent, vertically transmitted associations, THEORY-1214 — Cicada hosts whose endosymbiont Hodgkinia has split into many interdependent lineages compensate by sending more Hodgkinia cells to each egg, with Sulcia numbers and the transmission route unchanged, so that every egg still receives every lineage; the raised titre is a host adaptation driven by the symbiont's fragmentation, and a cost of it, THEORY-1215 — Besides Asgard archaea and the alphaproteobacterial ancestor of mitochondria, Myxococcota and Planctomycetota were major donors of genes to the eukaryotic lineage before its last common ancestor, in waves: Asgard first, then Planctomycetota before the mitochondrion, then the mitochondrial ancestor and Myxococcota together, THEORY-1219 — Buchnera's metabolism interlocks with its aphid host's: it makes the essential amino acids its host cannot from host-supplied glutamate and aspartate, depends on the host for the non-essential amino acids and its membrane phospholipids, and cannot live outside the bacteriocyte, THEORY-1223 — Monocercomonoides exilis lost its mitochondrion only after the organelle's essential functions had been removed in steps, Fe–S cluster assembly to a cytosolic SUF system and then the glycine cleavage system by loss, and the loss required no compensating change elsewhere in the cell, THEORY-1228 — A bacterial endosymbiont becomes genetically integrated, an organelle, when host proteins imported into it replace genes it has lost, and this does not require gene transfer from the endosymbiont: in the Paulinella chromatophore and the nitroplast, the two systems with hundreds of imported proteins, the replacing genes are mostly the host's own or come from other bacteria, THEORY-1235 — Losing a costly function whose product leaks to neighbours is favoured by ordinary individual selection in large free-living microbial populations, and the loss proceeds until the remaining producers just supply the community, so that most cells come to depend on a rare few with no relatedness, cooperation or collective required, THEORY-1243 — In incipient endosymbioses in nature, mutual dependence evolves ahead of reproductive cohesion, so that endosymbioses are more likely to be mutually dependent than cohesive
Cited as “refines” byQUESTION-353 — Across real symbioses, does the partner with the larger and faster-growing population become obligate first more often than chance, and does the other partner's dependence follow the balance of births and deaths inside the collective, as Athreya, Czuppon and Gokhale's model predicts?

Graph View

Why it is a question

The record has a theory of when a collective becomes an individual, and it has almost no cases of how partners come to depend on each other. Its readings set the conditions on the collective. Selection between collectives must come to trump selection within them (THEORY-141). Collaboration and generatively entrenched interactions must give organizational closure (THEORY-418). Darwinian and physiological individuality come apart (THEORY-443), and the reading reports Godfrey-Smith placing aphid–Buchnera as both. CLAIM-060 holds that constitutive dependence does not entail alignment of interests. What the record lacks is the biology of the routes by which partners lose autonomy. The exchange of 2026-10-27 named five, which “are not mutually exclusive”:

  • Adaptive gene loss. A costly, leaky function is lost because others supply it, and the loser becomes dependent (Black Queen, LIT-1568). Selection acts on the individual, not on the collective.
  • Drift-driven decay. Small, asexual, vertically transmitted populations accumulate mildly deleterious mutations (Muller’s ratchet, LIT-1573; reviews LIT-1559, LIT-1571). The resulting dependence need not benefit either partner.
  • Complementary loss across lineages. Pathways are split among nested symbionts and the host (LIT-1565), and a symbiont splits into two lineages with the functionality of one (LIT-1563). The number of dependent parts grows without an obvious new collective function.
  • Gene transfer and import. Genes move to the host nucleus and their products are imported back (Paulinella, LIT-1557; the nitroplast, LIT-1562; review LIT-1560). This route gives the host control.
  • Host compensation. The host maintains the collective’s function by transport, regulation or rescue, including with genes taken from third lineages (LIT-1569).

The exchange’s thesis, in its words: “A system can become more interdependent without becoming more cooperative, more unified, more autonomous, or even more adaptive.” Two of its cases show the routes do not run one way. In mealybugs the inner symbiont has been replaced repeatedly while host-encoded transferred genes stayed (LIT-1572). In Monocercomonoides a whole mitochondrion was lost once a bacterial Fe–S system replaced its one essential job (LIT-1567, LIT-1574). So losing genes is not the same as losing function, losing autonomy or gaining integration.

The exchange proposed scoring a partnership on five dimensions, as “a conceptual schema, not an established metric”:

  • D, physiological dependence. It is directional: the host’s dependence on the symbiont need not equal the symbiont’s on the host.
  • G, how essential functions are distributed across the genomes.
  • R, reproductive cohesion: co-transmission, synchrony, bottlenecks.
  • C, regulatory integration: the host’s control of transport, expression, division and allocation.
  • S, selection alignment: conflict within the collective relative to selection between collectives.

No single one is to stand in for individuality. Athreya, Czuppon and Gokhale’s model (LIT-1570) gives the first formal separation, of D from R. In it, mutual dependence evolves faster than reproductive cohesion even when investments in the two are uncorrelated. With a carrying capacity for collectives, complete dependence or cohesion may not evolve at all.

What would count as an answer. For each route, which of D, G, R, C and S it moves, shown on worked systems, not assumed. Then a stated criterion, tested on the same systems, for which combination makes a new evolutionary individual. The criterion must say whether high D with low R is a candidate individual or only a dependency. It must also say whether a partnership whose constituents keep being replaced is one individual or a succession. THEORY-418 predicts that metabolic complementation alone is not closure, and the mealybug patchwork is a place to test that. Eukaryogenesis is a harder test. The three phylogenomic programmes the exchange set together disagree on whether it was one two-partner merger or a sequence of associations: late mitochondrion after a complex host (LIT-1566), mostly Asgard inheritance (LIT-1558), and several waves of bacterial transfer (LIT-1561). LIT-1564 adds the chimeric metabolism. If the programmes disagree, the event may not have a single route at all. NOTE-159 already doubts that eukaryogenesis fits the transitions narrative.

Selection for extreme specialization within a group (Cooper & West, LIT-1225, unread) is a sixth route. It works within a species, where the exchange’s routes cross lineages.

The question is the exchange’s. The record takes no position on its answer until the works are read. A2 put it as follows: “The biological literature would not automatically settle these philosophical questions. It would, however, constrain what a successful theory of individuality must explain.”

Note of 2026-10-27 (later): cases, and works for what the exchange named without citing

Six documented cases now hold the systems the question names. All are Proposed, because their sources are unread.

  • Aphid–Buchnera (CASE-173): dependence produced largely by drift.
  • The mealybug’s nested symbionts (CASE-171): genes from third parties, and constituents replaced.
  • Hodgkinia’s splitting in cicadas (CASE-177): more parts and more dependence with no new function, and a host that compensates at transmission.
  • Paulinella (CASE-174) and the nitroplast (CASE-167): control through gene transfer and import.
  • Monocercomonoides (CASE-168): an organelle lost.

The exchange named several things without citing a work. Works now registered for each:

  • Gene transfer to the nucleus: LIT-1588.
  • Host compensation: LIT-1590.
  • Population-genetic models of gene loss: LIT-1611 and LIT-1616.
  • Metabolic-network constraints: LIT-1585.
  • Multitype branching processes: LIT-1608. This is a general text; no endosymbiosis work using the method was found.
  • Mutualism theory: LIT-1603.
  • Host control and within-collective conflict, the S and C dimensions: Frank’s two models, LIT-1617 and LIT-1605.
  • The eukaryogenesis scenarios A1 listed: syntrophy (LIT-1597, LIT-1591), and complexity before the mitochondrion (LIT-1595).

LIT-1605 makes a point that bears on the answer. Reproductive cohesion (R) can be imposed by the host’s control (C), by sequestering a germ line of symbionts. If so, the two dimensions are not independent, and an answer must say which drives which.

Note of 2026-10-27 (readings): what the first three readings say

Three of the four works the exchange called “Critical” have been read in full. The fourth, Moran 1996 (LIT-1573), is Unfetched: its free copy is behind a challenge this client could not pass.

  • The Black Queen route moves D one way and G, and nothing else (LIT-1568, NOTE-1212, THEORY-1048). Loss of a costly, leaky function is favoured until helpers just supply the community. No collective forms. There is no cohesion and no control, and the dependence runs from beneficiaries to helpers only. It is the record’s clearest case of interdependence that is not individuality. The paper states it for free-living microbes.

  • Past a genome-size threshold, G forces C (LIT-1571, NOTE-1213, THEORY-1049). Below about 400 kb a symbiont cannot build its own envelope, and below about 200 kb translation erodes. The host then presumably supplies membranes, transport and translation parts, with or without gene transfer. Host control can therefore be a consequence of the symbiont’s losses, not only of transfer and import. This couples two dimensions the question lists as separate.

  • D and R are separate, but their order is not settled (LIT-1570, NOTE-1211, THEORY-1050, THEORY-1051). This corrects the question’s summary and its “Why it is a question” section. Athreya et al.’s “mutual dependence evolves faster than reproductive cohesion even when investments in the two are uncorrelated” holds under their chosen mapping: free growth depends on a partner’s own obligacy, and dissociation on both partners’ adhesions. Their own appendix shows the bias disappearing under matched mappings and reversing under the opposite one. So which comes first is an empirical question about how the traits act.

    What the model does show robustly is the asymmetry and its sequel. The faster-evolving partner becomes obligate first. The other then stays, becomes fully dependent, or returns to independence according to births and deaths inside the collective. That gives the question one candidate variable for when dependence becomes individuality.

One open lead from the readings: LIT-1605 (Frank, unread) models host control of transmission. If a host can impose cohesion on its own, dissociation depends on one partner’s trait, and on Athreya et al.’s Table S1 the dependence-first bias largely goes. Reading Frank is the next step on the R and C dimensions.

Note of 2026-10-27 (batch 2): ten more readings

Ten more works have been read in full. The other 21 unread works in the cluster could not be fetched (11 Unfetched, 10 Unavailable; see their LITs).

Routes.

  • Transfer and import is mostly import (LIT-1560, NOTE-1241, THEORY-1100). In the two systems with import at scale:

    • the Paulinella chromatophore imports hundreds of proteins, “mostly from the host itself”, and transfer from the symbiont played “only a circumstantial role”;
    • the nitroplast imports more than 350, with no transfer from the symbiont found.

    So the route above (“Genes move to the host nucleus and their products are imported back”) is wrong as stated. Import moves C and G without the symbiont’s genes moving, and it shares third-party genes with the host-compensation route.

  • An order to test (THEORY-1107). Sørensen et al. propose:

    • host effectors first (C);
    • then dependence (D), when one redundant imported protein lets the symbiont’s gene decay;
    • then general import, which shifts G.

    Vertical transmission (R) is a condition: rhizobia are targeted by host peptides, are not transmitted vertically, and are not integrated. This reverses the insect order of THEORY-1049, where the symbiont’s losses come first. Neither order has been watched in one lineage.

  • Complementary loss moves G and the symbiont’s D, not C (LIT-1596, NOTE-1236, THEORY-1103). Buchnera keeps the pathways for the amino acids its host cannot make, and builds them on host-made precursors. It has lost its own regulators, which is not the same as being regulated. The genome paper names no mechanism of reduction; drift is LIT-1573’s account, which is Unfetched.

  • Host compensation maintains R, perhaps at a cost to C and S (LIT-1590, NOTE-1235, THEORY-1106). Cicadas send more Hodgkinia cells per egg as the symbiont splits, so every lineage still reaches every egg. The authors speculate that larger transmitted populations weaken bottlenecks and host control. If so, keeping R costs S, and an answer must say how the dimensions trade off. The rise is significant in one species of four.

  • Integration undone in steps (LIT-1574, NOTE-1243, THEORY-1098). Monocercomonoides lost its mitochondrion only after the organelle’s essential jobs went one at a time. First, Fe–S assembly moved to a SUF system that relatives with organelles share. Then the glycine cleavage system was lost. This is host compensation with a third lineage’s genes, run to dissolution.

  • No import below the tipping point. The host proteins seen inside insect symbionts are in Buchnera and Moranella, both above THEORY-1049’s thresholds (CASE-171, CASE-173). Host supply of tipping-point endosymbionts remains inferred.

Dependence stays directional even in an organelle. The nitroplast’s host can lose UCYN-A when given fixed nitrogen in culture (CASE-167). The symbiont cannot live without the host. D must be scored in each direction, as the question says.

Eukaryogenesis: the disagreement is narrower than stated above. The “Why it is a question” section set three programmes against each other on whether eukaryogenesis was “one two-partner merger or a sequence of associations”. The readings change that.

  • All three accept one endosymbiosis, an Asgard-related host with an alphaproteobacterium. All three also accept bacterial genes from other donors, some before the mitochondrion (LIT-1566, LIT-1558, LIT-1561, read in NOTE-1234, NOTE-1242, NOTE-1237).
  • Tobiasson et al. are themselves mitochondrion-late, so they agree with Kay et al. on order (THEORY-1104). Kay et al. argue against serial endosymbiosis (THEORY-1099).
  • The live dispute is between Tobiasson and Bernabeu. Are the other bacterial genes diffuse transfers or a few major donors in waves? And can stem lengths time acquisitions at all? Tobiasson et al.’s own test says mostly not (THEORY-1101), while Bernabeu et al.’s waves rest on them (THEORY-1105). Pittis and Gabaldón’s mito-late order rests on the same measure (LIT-1595, NOTE-1240, THEORY-1102).
  • No donor is shown to be a partner. Bernabeu et al. say their data “do not provide information on the host or endosymbiotic nature of any partner”. So “distributed” means distributed gene donors, not a series of collectives. For this question, the eukaryogenesis papers bear on G and not on R or S.
  • The metabolism is chimeric, but that does not single out syntrophy (LIT-1564, NOTE-1239, THEORY-1109). Any archaeal host taking up a bacterium with a TCA cycle predicts the split. The paper adds an instance of C: enzymes of non-alphaproteobacterial origin now work inside the mitochondrion. It also offers, as a possibility, a mechanism the routes above do not name: host genes duplicated and sent into the organelle “might have promoted the genome reduction of the endosymbiont”.
  • A dependence before any endosymbiosis (LIT-1591, NOTE-1238, THEORY-1108). The cultured Asgard archaeon grows only with interchangeable methanogen partners. That is high D with no R and no C: interdependence without individuality at the start of the story. In the authors’ E3 model the host makes the hydrogen, and they favour an interaction other than hydrogen transfer as the driver. So this case does not support the hydrogen hypothesis (LIT-1597, unread), and the previous note’s grouping of the two under “syntrophy” needs that caveat.

Note of 2026-10-29: Cooper and West, read

Cooper and West, LIT-1225, which “Why it is a question” lists as unread and as a sixth route, is now read (NOTE-1369). The route is asserted in the paper’s conclusion (“a driver, not a consequence”), not shown. The model ends at dependence, some individuals “completely dependent upon the helping behaviour of others”, and has no higher-level unit. The question is unchanged.

Note of 2026-11-04: West et al. 2015, read

West, Fisher, Gardner and Kiers (LIT-2003, NOTE-1538) give an order of conditions rather than of routes. The conditions of group formation come first, and align the partners’ interests: clonal bottlenecks, lifetime monogamy, vertical transmission of clonal symbionts. Mutual dependence comes later, “in most cases” through extreme division of labour. Drift is another route, with the host taking over roles a symbiont loses. Their criterion for a completed transition is mutual dependence together with negligible conflict, and Table 1 shows that neither suffices alone. They do not separate the remaining candidates, and they report “an almost complete lack of work addressing why certain traits are lost”. The question is unchanged.

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