Natural Sciences

Bacterial Expressions : Setting the tone

Editors’ note: This is the introductory post to the series ‘Bacterial Expressions‘ by Dr. Aswin Sai Narain Seshasayee on the fundamentals of molecular biology, microbiology and biochemistry underlying bacterial evolution.

Bacteria are everywhere, from the soil by our doorstep to the hottest thermal vents. They happen to be the predominant form of free-living life on this planet, with a population numbers of one followed by thirty zeros being bandied about. Even anthropocentrically, it has become cliched to state that the human body plays host to ten times as many bacterial cells as human cells, and that we will cease to exist in the absence of these creatures. Of course I do not have to make a mention of the flip side of being with bacteria – the numerous infectious diseases ranging from strep throat through tuberculosis to gastric cancer. But we may be best served by remembering that these disease-causing germs are only a minuscule fraction of all the bacteria that are there.

Many bacteria are obligate symbionts: they are dependent on their hosts for their survival, and in many cases where the host is biotic, the host and the bacterium have co-evolved such that their complementarity is astounding. At the other extreme are bacteria capable of surviving in many diverse habitats and in fact dominating them; their metabolic capabilities and the manner in which these abilities are regulated at the spatio-temporal level are remarkable.

It is not just a matter of metabolising nutrients; it is also a matter of facing up to stresses, from well, nutrient starvation, to evading the immune system of a large, well-accoutered host, to tacking toxicity of killing agents in the environment including those thrown at them by us in the form of antibiotics. And, just as we have a problem with viruses, so do bacteria, having to get around the problem posed in the form of predatory viruses called bacteriophages (or phages for short).

But bacteria have seen them all, and beaten most of them, and have learned to co-exist with others. It is a case of been there, done that for most bacteria. The objective of this series of articles is to present some fundamentals of molecular biology, microbiology and biochemistry, and to use this knowledge to present mechanisms by which bacteria evolve and how through genetic changes and transient regulatory mechanisms they approach the simple matter of taking over the big, bad world around them!

An electron micrograph of an individual Escherichia coli cell, the length of which is about one-thousandth of a millimeter (or a micrometre). Image prepared by Rajalakshmi Srinivasan, National Centre for Biological Sciences.

An electron micrograph of an individual Escherichia coli cell, the length of which is about one-thousandth of a millimeter (or a micrometre). Image prepared by Rajalakshmi Srinivasan, National Centre for Biological Sciences (

Readers are directed to the following website for interesting material on bacteria and microbes in general:

About the author

Aswin Sai Narain Seshasayee

I am a junior faculty working at the National Centre for Biological Sciences (

I did my undergraduation in Industrial Biotechnology from the Centre for Biotechnology, Anna University, 2005. Following a one-year stint as an Inlaks Foundation visiting scientist in Nick Luscombe's lab (then) at the EMBL-European Bioinformatics Institute, I continued my work as a PhD student in the same lab, under the aegis of the Faculty of Biology at the University of Cambridge and the International PhD Programme at EMBL. My PhD thesis has (what I think is) a self-explanatory title: "A computational study of bacterial gene regulation and adaptation on a genomic scale". Following a short bridging post-doctoral stint (rather un-adventurously in the same lab), I moved back to India - to NCBS, Bangalore - to establish a wet (experimental, in every sense of the word) / computational research lab investigating bacterial gene regulation and adaptation on a genomic scale.

My work in Cambridge was funded over the years by The Tucker Price Research Fellowhip at Girton College, Cambridge; The St. John's College Research Scholarship, Cambridge; The Developing World Education Fund and Dharam Hinduja Scholarship, Cambridge; University of Cambridge ORS award (now defunct); EMBL; The Inlaks Foundation; and BBSRC (through a grant awarded to Nick and Gillian Fraser, our collaborator).

I currently hold the Ramanujan Fellowship from the Department of Science and Technology, Government of India. I receive core funding from NCBS, our host institute. Extramural students are currently funded by Junior Research Fellowships from the Council for Scientific and Industrial Research and the University Grants Commission, and INSPIRE Fellowships from the Department of Science and Technology.


  • Awesome, looking forward to this series. One small request – at some point can you talk a bit about mitochondria having evolved from bacteria? I’m pretty sure it was never mentioned in my schoolbooks, and I found out about it only recently and my mind was blown. To me it was one of those things which, once you know, firmly establishes evolution as fact. Let’s make sure others know it as well!

    • A little history-of-science aside in this regard, is the remarkable story of Lynn Margulis. Quoting Prof. Jerry Coyne from this Edge retrospective on Lynn Margulis :

      All of us should honor Margulis’s real contributions to biology: her recognition and working out of earlier suggestions that some cellular organelles were acquired by symbiosis, and that the ancestors of these organelles were bacteria. This was a tremendous advance, achieved in the teeth of substantial doubt.

  • Thanks for the article.

    I have one question regarding the lifecycle of bacteria.

    What happens to these bacteria when host dies ?

    To be more specific, why bacteria or virus sometimes causes death in host? The purpose of any living things is to survive for long period of time. Let’s consider HIV, in that case when HIV +ve person dies, the virus is also killed. Eventually, if all the host are infected (this is far fetched but could happen) and died then virus itself will die out.

    Maybe, the before killing the host the virus will mutate to non-lethal variant and survive. But why kill in first place ?

    Any collective consciousness in virus or bacteria ?

    • I am not up to speed on literature on this. But here are my two pennies (not exactly well thought out though):

      (a) Some pathogens are generally crippled and slow growing. They will simply find it difficult to outcompete the friendly microbiota of the host. The only way for them to survive is by causing damage to the host; disease may be an unanticipated outcome. And successful, chronic pathogens (incl. HIV) do spend a long time in their host before doing any fatal damage.

      (b) Other pathogens can survive in multiple habitats. Pathogenesis may be a way to propagate.

      But, please do wait. I will come up with a proper survey of literature on this at some stage.

      I do not know what “collective consciousness” means!

      • For “collective consiousness” means, that how could bacteria/virus mutate to non fatal variant. The survival of the fittest may be applied here. But how these micro-organism mutate so fast ( is this bcz they grow tooooo fast) ?

        Thanks for the comment. Waiting for next installment on this series…:)

    • Nice article Aswin. one of the worst taught subjects in India is biology. Your effort to give a perspective in bilogical areas is much appreciated. Wiating for the rest of the series.

  • Sir,
    Please explain abt the dimensions, how to see them (i.e) if you say there is bacteria, explain us how to see it is there. Please explain to the finer details so that we could enjoy its life.
    thanking you,

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