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Losers win when the sugar changes
Put a flask of bacteria in glucose, the simple sugar that goes in coffee, and the colony grows into billions or trillions of cells. Some grow very fast. A few almost always divide slowly, and the system keeps producing them anyway.
Take a little of that culture and move it into galactose, a milk sugar. The fast growers that won in glucose often stop winning, and the new leaders emerge from the loser pool.
That is fitness that comes from diversity of genes in a crowd, and it reaches into human health. Genes that make some people susceptible to a disease can help in a different setting. The sickle cell gene is defensive against malaria, and it is common in people with sub-Saharan African origins. Mild psoriasis, an autoimmune condition, could come with better resistance to infection, which shows how autoimmunity can be useful.
Why do bacteria keep slow growers around?
Producing a mix of fast and slow growers is a strategy called bet hedging. Slow growers do poorly when food is plentiful, but they survive when conditions turn harsh. In 1944, Joseph Bigger found that penicillin killed nearly all of a staphylococcus culture while a few dormant survivors remained, which he called persisters. When the antibiotic was removed, the survivors regrew a full population.
Why does a change of sugar stall bacteria?
In the 1940s, Jacques Monod grew E. coli on mixtures of sugars and saw two bursts of growth with a pause between them. The bacteria first used up glucose, then needed time to switch on the genes that handle the second sugar. Monod and François Jacob later described the lac operon, the genetic switch that controls the use of lactose. The cells that handle the change fastest regain the lead.
How does the sickle cell gene protect against malaria?
A person who inherits one copy of the sickle cell variant makes some abnormal hemoglobin along with normal hemoglobin. Red blood cells infected with the malaria parasite tend to sickle and get cleared, which limits how much the parasite can grow. Two copies cause sickle cell disease. A. C. Allison proposed this protective link in 1954 after noting that the variant was common in regions where malaria was widespread.
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