Evolution can be defined as the modulation of a set of inherited characteristics of individuals by environmental conditions. In this definition, the characteristics that fit the compromise of the species and the environment best, are those that survive in a given species.

This applies to microbes, also called single-celled organisms, as well as much to larger, multi-cellular organisms such as humans. Perhaps partly because they are so small, and thus can be dispersed easily, microbes are more diverse than any other group of living organisms. They span two domains of life, archaea and the more familiar bacteria.

The theory of evolution explains the existence of this variety as the exposure of single-celled organisms to a great variety of conditions (virtually the whole of the Earth) over a considerable time scale (billions of years). We are therefore not at all sure we know what all of these microbes are. We are only tentatively sure of the extent of the environment in which they live. Archaea, the third domain of life sometimes called extremophiles, were formally described as late as the 1970s. New bacteria are discovered every day—some in the Amazon rainforest, and some in hospitals in which antibiotics have been prescribed too much.

Such a range of bacteria would not survive if they could not also live within certain changes in their own environment. Such changes include the seasons and thus wet and dry conditions, as well as warm and cold. These are important for the cells to cope with as they affect the availability of nutrients, oxygen and sunlight. They also affect the amount of warmth available. We associate this with comfort—it’s nicer to be in a warm place than a cold one, only a very few people seek to go somewhere cold on holiday purely for that reason. However, there is also a thermodynamic reason. Warmer rather than less warm is a change in the thermal energy available, something that changes the behaviour of the molecules that constitute cells.

When energy is lower, cells are typically less active. However, cells that survive are ones that can still live, and better still grow, under such conditions. Hardy microbes therefore have mechanisms for coping with the cold, that can be called upon when the temperature drops. Yeast is one such microbe. It has also found use as a research tool because it is a eukaryotic cell that has only about 5k genes and can be manipulated genetically and grown in a laboratory.

The form of yeast known as Saccharomyces cerevisiae, is the principal sort studied in laboratories. It has evolved the ability to grow under cold conditions. In fact, it has recently been discovered that a key part of this adaptation is the result of a single gene. Study of a strain of S. cerevisiae with a mutation of its inp51 gene have shown that a major signalling lipid called PIP2 is linked to both membrane fluidity and cell growth. This suggests that membrane fluidity is key to the survival of S. cerevisiae under cold conditions.

Córcoles-Sáez et al. showed that S. cerevisiae with the mutated inp51 gene had a lipid fraction around 40% smaller than that of the unmutated form (wild type), and moreover that the membrane that was there was less fluid [1]. This showed that this gene influences not only the size of the lipid fraction but also what it contains. The size of the fats fraction (triglycerides) was reduced still further, by around 68%. This implies that this gene is involved in the synthesis of all fatty-acid-containing biomolecules. This is because it affects the abundance of both energy storage molecules (fats) and structural molecules (lipids) that comprise fatty acids.

Although spectroscopic determination of the lipid profile has only been applied to the wild type S. cerevisiae [2], it seems clear from chromatographic data alone that there are differences between the two strains, especially in the larger bulk-lipid fractions such as PC and PE [2]. This underscores the fundamental nature of the shift to lipid metabolism.

This raises the question of what the mechanism is between this gene mutation and the lipid fraction. The inp51 gene encodes for a phosphatase (enzyme) that turns PIP2 into another lipid, PI-4-P. This enzyme therefore catalyses the removal of a phosphate, which has the biological effect of turning the PIP2 lipid signal off. This also means that PI-4-P is not made, the effects of this lipid are not observed, thus probably limiting the extent of stored curvature elastic stress [3]. This suggests that PIP2 restricts phospholipid synthesis, and thus may be of use during periods where the cell needs to change or perform some other function, rather than to grow or repair itself.

This represents an extraordinary level of influence for a single gene. The ability to turn off this lipid signal influences an entire fraction of the cell, almost an entire type of biomolecule it possesses. However, it also indicates that the ability to control PIP2 has a profound effect on the cell.

It also brings out yet another question. What else might control acclimatisation to the cold? Indeed, is there anything? The answers to these questions would tell us how such microbes perceive colder conditions, as well as what they require to live in them.


[1] I. Córcoles-Sáez, M. L. Hernández, J. M. Martínez-Rivas,
J. A. Prieto, F. Randez-Gil, Biochimica et Biophysica Acta, 2016, 1861, 213. http://dx.doi.org/10.1016/j.bbalip.2015.12.014.

[2] C. S. Ejsing, J. L. Sampaioa, V. Surendranatha, E. Duchoslavb, K. Ekroosc, R. W. Klemma, K. Simonsa, A. Shevchenko, Proceedings of the National Academy of Sciences, 2009, 106, 2136. http://dx.doi.org/10.1073/pnas.0811700106

[3] S. Furse, N. J. Brooks, A. M. Seddon, Rudiger Woscholski, R. H. Templer, E. W. Tate, P. R. J. Gaffney and O. Ces, Soft matter,2012, 8, 3090-3093. http://dx.doi.org/10.1039/c2sm07358g