Source
Karnkowska et al. (2019), Molecular Biology and Evolution 36(10): 2292–2312, LIT-1574, read in full in NOTE-1243 from the PubMed Central copy. “Is the Absence of Mitochondrion Reflected in Modifications of Any Cellular System?”, the FIB-SEM section, and the conclusions.
What was actually shown
- No organelle seen. FIB-SEM of two cells, fixed two ways, found no mitochondria or MROs. The authors “acknowledge that the resolution of the microscopy could still allow for undetected highly reduced mitosomes”.
- Two preadaptations, by distribution among relatives.
- “The ISC pathway, otherwise considered to be an essential house-keeping pathway in eukaryotes, was functionally replaced in all examined Preaxostyla by the SUF pathway”. A full set of essential Fe–S proteins (70 candidates) is served by the cytosolic SUF and CIA systems.
- M. exilis lacks the glycine cleavage system and SHMT, “which are both present in its close relative Paratrimastix pyriformis, where they localize into the MRO”. Their loss “removed another essential function from the MRO …, preadapting it for loss of the organelle”, and “took place after the split from the P. pyriformis lineage”.
- One concomitant loss. No mitophagy or pexophagy orthologs: “an example of a system likely lost together with mitochondria”. Peroxisomes are also gone but are lost in many anaerobes.
- No postadaptation. Energy metabolism resembles that of mitosome-bearing anaerobes, with “no indication that they were affected by the complete loss”. None of the functionally annotated genes unique to M. exilis is “clearly related to the loss of mitochondrial function”. The cytoskeleton, kinetochore, membrane trafficking, autophagy, oxidative stress response, calcium flux and metabolism are not “significantly altered relative to eukaryotes with mitochondria”.
What could have failed: the genome could have been reduced or unusual in ways tied to the loss, such as new cytosolic versions of mitochondrial pathways or a collapse of the systems that interact with mitochondria. The SUF replacement could have been unique to M. exilis, making it the single trigger.
What this does not say
- Not that SUF alone made the organelle dispensable. It is shared with relatives that kept MROs. The 2016 framing, a single preadaptation, is widened here to two.
- Not when the steps happened. The order comes from which relatives have what. No step is dated.
- Not what the last MRO did. The paper names no function remaining after GCS and SHMT were gone.
- Not that the cell has no mitosome. Below FIB-SEM resolution, the question is open.
- Not that the lost organelle was replaced. The functions were replaced or dropped; nothing took the organelle’s place as a compartment.
- Not that complex cells existed before the mitochondrion. That is the paper’s closing suggestion, from a secondary loss.
Connections
- QUESTION-277. The negative control, made more exact. The partner’s functions were moved to a third-party gene or dropped until no dependence on the partner remained, and then the partner was lost. It is the host-compensation route run to dissolution, and it says that integration as deep as a mitochondrion’s can be undone one function at a time. The reading in the question’s terms is mine.
- CASE-168. The case’s “one indispensable job” should read “two essential functions, removed in turn”.
- THEORY-1100. Organelles are made by moving functions onto host-encoded proteins. This is the same accounting from the other end: the organelle persists while some function still needs it.
- THEORY-1049. McCutcheon et al. find the host supplying what a shrinking symbiont lacks. Here the host supplies everything the organelle once did, and the organelle goes.
Note of 2026-10-30: promoted, and the wider thesis filed beside it
The twenty-second status review promoted this reading under ADR-065: it reports what Karnkowska and colleagues’ genome analysis finds and infers, and NOTE-1243 read the paper in full. Whether Monocercomonoides lost its mitochondrion in this way is THEORY-1223’s question, Proposed, which keeps this entry’s old promote_when.