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    Drug-resistant bacteria protect the vulnerable microbes

    The long-held notion on how bacteria develop resistance to antibiotics stands challenged.

    The conventional thinking is that continuous exposure to antibiotics or exposure at sub-optimal

    levels can facilitate some bacteria to develop mutations that render them resistant to a particularantibiotic. And this antibiotic-resistant mutation is then passed on to succeeding generations, and

    in time the antibiotic-resistant bacterial population becomes dominant.

    But a paper published today (Sept 2) in Nature reveals how drug-resistant mutants resort to a

    quicker way to make the overall population of bacteria resistant to a particular antibiotic in thevery same generation.

    Helping hand

    The antibiotic-resistant mutants lend a helping hand to protect other drug-susceptible species, the

    study shows. This is the first time a study has shown that drug-resistant mutants need not becomethe dominant species to become a threat. Surprisingly, the mutants protect the entire population

    even though it is at some cost to themselves.

    The study also highlights the danger of using antibiotics at sub-optimal levels.

    A study done in a bioreactor used the drug, Norfloxacin, at lower concentrations than was

    actually required to kill Escherichia coli bacteria. In fact, the dosage of the drug was chosen suchthat only 60 per cent of growth was inhibited.

    Still survived

    The concentration of the drug was increased every day. Surprisingly, despite increasing thedosage on a daily basis, even the bacteria that had not developed the drug-resistant mutation, and

    therefore had low-resistance to the drug, still managed to survive.

    Even on day nine, the bacteria with low-resistance survived despite the fact that the drugconcentration was much higher than what was required to kill the bacteria. The researchers note

    that a vast majority of individual E. coli were less resistant to the drug than the population as awhole.

    They also found that the norfloxacin-resistant mutants increased in number first, followed by an

    overall increase in the population of low-resistance E. coli.

    So how was this achieved? A few highly resistant mutants improve the survival of the

    population's less resistant constituents, the researchers note. And this was through theproduction of a small signalling molecule called indole that improves stress tolerance (in this

    case, the ability to survive the drug) in E. coli.

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    We propose that indole produced by the drug-resistant mutants was protecting its less-resistantneighbours, the authors write.

    Role of indole proved

    To further ascertain the role of indole, the researchers added the molecule and found those E.coli, which had low-resistance to the drug, increased and survived at drug concentrations thatwere many times more lethal.

    The results were the same when the experiment was repeated using a different drug gentamicin.

    This shows that the mechanism by which the drug-resistant mutants protect the rest of the

    population is the same, immaterial of the drug in question.

    Gecko-inspired robot to scale smooth walls

    Using the biology of a gecko's sticky foot, a robot that climbs in the same way the small reptile, gecko, can scale a

    wall of slick glass, with feet modelled on the intricate design of gecko toes is being developed.

    Sun's UV levels affect our outer atmosphere

    Large shifts in the sun's energy output may drive dramatic fluctuations in Earth's outer atmosphere. A recent,

    temporary shrinking of a high atmospheric layer is linked to a sharp drop in the sun's UV radiation.

    SOFIA will shed light on universe's mysteries

    How were millions of young stars able to form at the centre of our galaxy in the presence of a black hole with a

    mass 4 million times that of the sun? This and other questions may be answered by the NASA mission SOFIA.

    Grapefruit's promise for diabetes therapy

    Naringenin, an antioxidant derived from the flavor of grapefruits and other citrus fruits, may cause the liver to

    break down fat while increasing insulin sensitivity, a process that naturally occurs during long periods of fasting.