When developing modern systems, mankind is very adept at putting in place contingency plans. They are there to anticipate events rolling out of control or to prevent significant loss or damage. Sometimes they are effective, many times, however, they prove to be totally inadequate. The point, though, is that these alternative plans suggest thoughtfulness and purpose. They are there in anticipation of events that may go wrong. They are there as an outcome of forethought and expectation.

There is evidence of similar forethought and planning within nature. There are accidents in biology that don’t always happen but might happen. When they do, systems are invariably in place that fly into action and do what needs to be done. A person might go for years without a cut or scratch, but the contingency plan is there anyway, just in case. Here are some recently known examples of contingency planning within the cell itself.


Collagen is the most abundant protein in the human body. When collagen fibres are assembled, there’s a polysaccharide that usually sits idly by. It is called N-glycan, and its role has remained elusive for decades. Rasia C. Li et al., publishing in PNAS (Proceedings of the National Academy of Sciences of the United States of America), have helped discover why it is there. It is essential for collagen folding and secretion when disease is present or when tissue needs repairing.

Collagen fibrils often fold properly without the help of N-glycan. When folding is about to go awry, though, Nglycosylation calls in chaperones that rush in like spotters for a gymnast, making sure the growing collagen fibril doesn’t hurt itself and the organism.  This molecule’s function, therefore, demonstrates contingency planning—only coming into operation when normal folding breaks down.

Too much light

When sunlight is adequate, leaves are content. Their photosynthetic antennae direct the energy into the photocentres for conversion to food molecules. On some days, though, there can be too much of a good thing. Like sunburned beachgoers, plants too can burn, but they lack the ability to run to the shade. There’s a contingency plan for that situation.

In PNAS, Jacob S. Higgins et al. describe how “Photosynthesis tunes quantum-mechanical mixing of electronic and vibrational states to steer exciton energy transfer.” Quantum mechanics is “the branch of mechanics that deals with the mathematical description of the motion and interaction of subatomic particles, incorporating the concepts of quantization of energy, wave–particle duality, the uncertainty principle, and the correspondence principle.” According to scientists the humble plant is a master at utilising these principles like an overflow valve, steering excess energy into a quenching centre.

What they discovered was that photosynthetic light-harvesting antennae on the leaves transfer energy toward reaction centres with high efficiency, but in high light environments, these antennae divert energy to protect the photosynthetic apparatus. Amazing when you think about it! How would blind chance even know of the existence of light, let alone develop complex processes to convert light to food. And how would blind chance know that leaves would need to protect themselves from too much light and assemble a quantum-mechanical mixing of electronic and vibrational states to divert excess energy away from sensitive areas of the plant? If the process of photosynthesis was not working from day one, then plants would not have been able to survive at all.

DNA’s repair toolkit

Chinese scientists at the Peking University Health Science Centre examined the critical pathways that cells use to avoid cancer or genomic instability. A chart of five repair pathways was posted by Medical Xpress, under the headline, “Understanding the DNA repair toolkit to chart cancer evolution”. This chart shows five repair systems that protect DNA from damage. These are contingency planning systems that are ready and waiting to step in, like EMTs (epithelial-to-mesenchymal transition), when things go wrong during cell division or transcription. There are five systems they discussed:

  • Mismatch repair fixes mutations that insert the wrong base
  • Nucleotide excision repair comes to aid when DNA structural damage occurs
  • Base excision repair fixes bases that become separated from the strand
  • Double-stranded break repair solves the complex situation when both DNA strands become separated
  • Inter-strand crosslinks repair helps when drugs block replication and transcription

When these systems work properly, they can prevent cancer and drug resistance. Many life-threatening diseases are prevented by these five pathways. When the pathways themselves fail, though, it can be bad news for the organism. The Chinese team felt that systematising our knowledge about these pathways and the specific consequences of “pathway damage” can help oncologists know which avenues provide the best therapies for specific cancers.

Cell leakage

Origin-of-life theorists often assume that cell membranes would spontaneously form naturally around proto-cells by the properties of lipid self-organisation. This is indeed wishful thinking, because the formation of a membrane which carefully controls what goes in and out of cells is a sophisticated balancing act of regulating ions and proteins. But, in addition to that, there are repair mechanisms which kick into place when a cell membrane breaks.

A paper in The EMBO Journal by Yan Zhen et al., “Sealing holes in cellular membranes”, describes how cells actively monitor and repair leaks. The authors state that 20-30 percent of muscle cells and 6 percent of skin cells present transient leaks in their membranes that must be sealed promptly, or else serious diseases can occur.

A cell must have ways to know that a leak has begun. A rapid influx of Ca2+ ions triggers a “simple yet powerful mechanism for detection of membrane integrity.” This, however, requires the presence of proteins that bind to the calcium ions so that they can trigger mechanisms that “promote membrane sealing by membrane fusion, fission or tension reduction.”

A table in their paper lists at least 16 proteins and protein families that promote membrane sealing in four categories of damage. Annexins, for instance, gather at the site of damage and “assemble into multimeric structures that physically cap the hole in the membrane.” Another protein, named dysferlin, “accumulates phosphatidylserine at the site of membrane damage, as an ‘eat‐me’ signal for macrophages.” Dysferlin also “interacts with some annexins” indicating that membrane repair proteins are not acting alone, but, like an enzyme army, form networks of players that work together. Cooperation between proteins that can solve problems multiplies exponentially the improbability of their spontaneous emergence by unguided natural processes.

The article highlights the fact that PDCD6 (a calcium-binding sensor) has 865 amino acids. These are not small players! A whole squadron of machines takes part in healing membrane holes, just like an army of players is required in the blood clotting cascade to repair breaks in blood vessels. There are additional machines involved in repairing internal membranes surrounding organelles and the nucleus. Different types of holes receive different types of sealing mechanisms.


In these four examples, we have systems in place which suggest foresight. They are there to ensure the successful operation of cellular systems in the face of numerous potential threats. It is inconceivable that evolution could anticipate things going wrong by supplying contingency processes just in case the original evolved process is broken! Alternative mechanisms, anticipating the need to repair or mitigate, suggest forethought and planning. Contingency planning is surely evidence of design and wisdom. As the psalmist said, “in wisdom thou hast made them all.”