Editor’s note: The Focus on Research column highlights different research projects and topics being explored at Penn State. Each column will feature the work of a different researcher from across all disciplines. The following is the second of a two-part installment that originally appeared on The Conversation.
Whether the final number of human genes is 20,000 or 3,000 or something else, the point is that when it comes to understanding complexity, size really does not matter. We’ve known this for a long time in at least two contexts, and are just beginning to understand the third.
Alan Turing, the mathematician and WWII code breaker, established the theory of multicellular development. He studied simple mathematical models, now called “reaction-diffusion” processes, in which a small number of chemicals — just two in Turing’s model — diffuse and react with each other. With simple rules governing their reactions, these models can reliably generate very complex, yet coherent structures that are easily seen. So the biological structures of plants and animals do not require complex programming.
Similarly, it is obvious that the 100 trillion connections in the human brain, which are what really make us who we are, cannot possibly be genetically programmed individually. The recent breakthroughs in artificial intelligence are based on neural networks; these are computer models of the brain in which simple elements — corresponding to neurons — establish their own connections through interacting with the world. The results have been spectacular in applied areas such as handwriting recognition and medical diagnosis, and Google has invited the public to play games with and observe the dreams of its AIs.
Sign Up and Save
Get six months of free digital access to the Centre Daily Times
Microbes go beyond basic
So it’s clear that a single cell does not need to be very complicated for large numbers of them to produce very complex outcomes. Hence, it shouldn’t come as a great surprise that human gene numbers may be of the same size as those of single-celled microbes like viruses and bacteria.
What is coming as a surprise is the converse — that tiny microbes can have rich, complex lives. There is a growing field of study — dubbed “sociomicrobiology” — that examines the extraordinarily complex social lives of microbes, which stand up in comparison with our own. My own contributions to these areas concern giving viruses their rightful place in this invisible soap opera.
We have become aware in the last decade that microbes spend more than 90 percent of their lives as biofilms, which may best be thought of as biological tissue. Indeed, many biofilms have systems of electrical communication between cells, like brain tissue, making them a model for studying brain disorders such as migraine and epilepsy.
Biofilms can also be thought of as “cities of microbes,” and the integration of sociomicrobiology and medical research is making rapid progress in many areas, such as the treatment of cystic fibrosis. The social lives of microbes in these cities — complete with cooperation, conflict, truth, lies and even suicide — is fast becoming the major study area in evolutionary biology in the 21st century.
Just as the biology of humans becomes starkly less outstanding than we had thought, the world of microbes gets far more interesting. And the number of genes doesn’t seem to have anything to do with it.
Sean Nee is a research professor of ecosystem science and management at Penn State.