Part of the cell · Essential stress protection
Surviving oxygen damage
Not labelled on the cell picture.
Oxygen is this cell's fuel partner and also its poison. These proteins mop up the reactive by-products. Notably, this genome has no catalase at all, so a single route carries the whole load.
Proteins in the model: 62
Part of the model's 1051 proteins. Each group below is a book group, counted in the working count after the repeats and non-first-cell groups were removed. The proteins are not yet matched gene by gene.
| Group | Proteins |
|---|---|
| Defence set (B1) | 26 |
| Stress response system | 10 |
| Bacterial-Host Interactions | 3 |
| ROS management | 5 |
| Proteolysis pathway | 3 |
| Proteolytic systems | 5 |
| Lon protease | 1 |
| Metalloprotease pathway | 3 |
| Serine protease pathway | 3 |
| Peptidase pathway | 3 |
Its pathways
- Damaged-protein turnoveratlas pathway3
- Peroxide and superoxide handlingatlas pathway2
- Not yet placed in a pathwayto sort2
If it fails
Damage outruns repair. Not fatal in one generation, but the lineage dies out.
Damage accumulates · over several generations
What it depends on
- Quality control (not a separate group in the tree)Folding, rescue, and degradation systems mitigate stress-induced molecular damage.Book pp. 302–303, 503–505
- Turning hydrogen into usable energyEnergy supply supports many protective, repair, and protein-turnover responses.Book pp. 499, 505
- Reading genes into RNA, Building proteins and folding themTranslation replaces damaged proteins and produces stress-response factors.Book pp. 501–502, 505
What it supplies
None listed in the curated set.
Dependencies are curated from the book at the level of the map’s systems and are not measured protein contacts. See all systems together.
How it is built and controlled
Counts from UniProt annotations of this group’s proteins.
Its place in the control layer
None of this group’s proteins appear in the information, signaling, regulation, machine-signal or assembly lists.
From the control-layer pages. Which genes a regulator controls is mostly inferred from related bacteria, because Aquifex has no genetic system for testing it directly.
Origins
What needs to be explained
How did persistence under fluctuating conditions, chemical damage control and repair become compatible in early systems?
What needs explaining. Explain protective chemistry and inducible responses appropriate to actual historical stresses, without treating modern exposure-specific pathways as first-cell necessities.
Hurdles
- H-STR-1Environmental exposureThe problem. The cell's setting brings heat, ultraviolet light, reactive oxygen and toxic metals.Why it is hard. Each of these damages proteins, nucleic acids and membranes, and the specific agents depend on the setting assumed.Chemistry before lifeStage 0: Not yet addressed by experimentShown: not yet addressed by experiment.In the books: 54 open problems on stress response ↗
- H-STR-2PersistenceThe problem. Proteins, RNA and energy carriers must last long enough to be useful.Why it is hard. High temperature speeds up the breakdown of RNA, ATP and peptide bonds; at the temperatures where Aquifex lives, many such molecules last minutes to hours.Chemistry before lifeStage 2: One step shown on its ownShown: Mineral surfaces and vesicles can slow the breakdown of some fragile molecules.In the books: 54 open problems on stress response ↗
- H-STR-3Protection trade-offsThe problem. Protection must shield the cell without cutting it off from the resources it needs.Why it is hard. Barriers that keep out damaging agents also keep out nutrients; protection must be selective.The integrated cellStage 0: Not yet addressed by experimentShown: not yet addressed by experiment.In the books: 54 open problems on stress response ↗
- H-STR-4TurnoverThe problem. Damaged molecules must be removed and replaced faster than damage accumulates.Why it is hard. Replacement costs energy and materials and depends on the synthesis machinery being intact.The integrated cellStage 0: Not yet addressed by experimentShown: not yet addressed by experiment.In the books: 54 open problems on stress response ↗
- H-STR-5Encoded protectionThe problem. Protective enzymes (superoxide dismutase, peroxidases, chaperones and repair enzymes) must be specified by genes and made when needed.Why it is hard. Protection must be present before damage occurs, and the instructions for it must pass to every daughter cell.Information and controlStage 0: Not yet addressed by experimentShown: not yet addressed by experiment.In the books: 54 open problems on stress response ↗
Scope. The severity of a hurdle depends on exposure. Modern oxidative defenses cannot be imposed unchanged on every proposed early-Earth setting.
Experimental progress. Experiments in Escherichia coli show that hydrogen peroxide can damage selected iron–sulfur enzymes and interfere with metabolism, linking protective chemistry to continued enzyme function.
What would strengthen a natural account. Steps shown to work together under plausible early-Earth conditions, without a chemist choosing the reagents, purifying the products or changing conditions between steps, would strengthen a natural account of origins in proportion to what they explain. Loss of a claimed dependency or discovery of functional alternatives would weaken the corresponding design argument. Gaps in the record do not supply a numerical likelihood for either explanation.
Observations. Stress recognition and regulation can change protective activity. Damage can require refolding or degradation, depending on the lesion.
Hallmarks that apply.
- H38 Environmental sensing: Stress recognition and regulation can change protective activity.
- H34 Protein quality control: Damage can require refolding or degradation, depending on the lesion.
- H39 Defense and surveillance: Threats such as viruses and foreign DNA are identified and neutralized, and damage is repaired.
The author’s conclusion. The coordinated features give the author a positive reason to consider design within the wider cellular architecture. For this local system alone, they do not establish that design is uniquely the best historical explanation. The conservative inference is that the system contributes to a cumulative design case, with its weight conditional on the comparative evidence and on how much plausible natural pathways explain.
From the book article Stress Response, with its scientific references.
How it was discovered
- 1969McCord and Fridovich discover superoxide dismutase, the first enzyme known to remove a reactive form of oxygen.McCord & Fridovich, Journal of Biological Chemistry 244:6049–6055 (1969)
- 1973Yost and Fridovich purify an iron-containing superoxide dismutase from E. coli, the type Aquifex uses (sodB).Yost & Fridovich, Journal of Biological Chemistry 248:4905–4908 (1973)
- 1989Jacobson and colleagues describe alkyl hydroperoxide reductase (AhpC), which protects DNA from oxidative damage.Jacobson et al., Journal of Biological Chemistry 264:1488–1496 (1989)
- 1995FtsH is shown to be a membrane-bound, ATP-dependent protease that removes specific proteins.Tomoyasu et al., EMBO Journal 14:2551–2560 (1995)
- 2014A review of the evidence dates the first lasting rise of oxygen in the atmosphere to about 2.4 billion years ago. Before that, reactive oxygen came mainly from sunlight and radiation acting on water.Lyons, Reinhard & Planavsky, Nature 506:307–315 (2014)
Each hurdle above is sorted by kind and by how far experiments have got (see “How hurdles are sorted” at the top).
All parts of the cell side by side: origins hub. The book articles:
- Stress Response: system page · full description · origins