Indy (I’m not dead yet)

DrosophilaI take my hat off to the original inventors of Drosophila gene nomenclature. They managed to create names that are clear descriptions of the genes effect, are easy to remember, and express something of the humanity of the scientists behind the discovery. Once you’ve heard it, you can’t forget that Cleo (Cleopatra) is only lethal in the presence of Asp, or that in tinman, the embryo has no heart. I really appreciate the ease-of-use of FlyBase and the incidental entertainment value of many of the Drosophila gene names.

My all-time favorite Drosophila gene name is Indy (I’m not dead yet). I just can’t get the image of loudly complaining flies in a wheelbarrow out of my mind. So it was with some consternation that I learned that there has been some debate over the past couple of years as to whether the Indy mutation is indeed responsible for increased lifespan (Toivonen et al 2007).

While researching citations that use our Maxwell 16 DNA Purification Kits, I was interested to come across the paper Long-lived Indy and calorie restriction interact to extend life span (PNAS 106, 9262-7), which sheds further light on the interesting relationship between Indy expression and aging. Calorie restriction has long been associated with enhanced lifespan in several species, including rats, flies, and nematodes. The authors of the PNAS paper showed that normal flies on a calorie-restricted diet had reduced Indy expression and enhanced lifespan. Indy mutant flies fed a normal diet also had a longer lifespan, which could not be enhanced further by calorie restriction. So the mutation in the Indy flies had the same effect as calorie restriction in normal flies. Also, the Indy mutants and the calorie-restricted normal flies both exhibited characteristics typically associated with calorie restriction, such as reduced insulin signaling, sensitivity to starvation, and lack of weight gain. Indy mutants had normal absorption of food, so the mutation itself did not cause calorie restriction by reducing the ability to intake food. This study shows a strong relationship between food calorie content and Indy expression, and suggests that calorie-restriction and Indy expression interact to cause the observed increase in lifespan. In the discussion, the authors suggest that identification of molecular targets shared between Indy and calorie restriction may provide further insight into why calorie restriction results in lifespan extension in Drosophila.

So it looks like Indy won’t be in for a name change any time soon.

In related news on aging research—a paper was published last week in Science showing that calorie restriction may be associated with longevity in primates. The bottom-line message from this 20-year study of monkeys on a restricted diet is simple: Consuming fewer calories leads to a longer, healthier life. Researchers from the University of Wisconsin reported that a nutritious but reduced-calorie diet significantly delays the onset of such age-related disorders as cancer, diabetes, cardiovascular disease and brain atrophy. … > read full article

Is anyone else besides me hoping that an Indy-like gene will be discovered in one of these skinny people who can eat what they like and not gain weight? Even as the data mount, I don’t think the calorie-restriction lifestyle option is going to work for me…….

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Isobel Maciver

Isobel Maciver

Isobel is a graduate of the University of Edinburgh and of Aston University in Birmingham, U.K. She is a technical writer and editor, and is also manager of the Scientific Communications group at Promega. She enjoys writing about issues in science and communication.


  1. Some of my favorite gene names come from the research on Drosophila to identify mutants that are more or less sensitive to alcohol. My favorite is “cheap date” a sensitive mutant, but I “tipsy” and “barfly” are pretty good too.

  2. The only problem comes in when someone gets a mutation in one of these genes and they have to be told that the problem is due to a mutation in cheap date… So yeah, these names are great if the human homologs don’t adopt the same name.

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