The paper "Transient Exposure to Low Levels of Insecticide Affects Metabolic Networks of Honeybee Larvae " is well done.  The research was careful, thorough, and the authors were conscientious about cross-checking the results of the molecular techniques they used in order to confirm any variations in the results.  This is important because the methods are very sensitive, and since variations among genetically-different individuals are normal, overall effects are subtle.  In order to ensure that observed overall effects are real, therefore, multiple assessment methods are needed.

I am not an expert in, nor do I perform RNA-Seq, multiplexed RT-PCR, or other molecular methods employed in this paper.  I do, however, understand how they work and what they are supposed to show.  I was struck by this observation in the paper:

"Overall diminished Hsp90 RNA levels in IE larvae was also detected by multiplexed RT-PCR using additional larval samples (Figure 3<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068191#pone-0068191-g003>). Reduction of Hsp90 levels would be a strategically sound response to a new environmental stressor. It allows the release from – and expression of – pre-existing cryptic genetic and epigenetic variants. Some of these variants may improve the chances of normal larval development, while others will increase imidacloprid sensitivity, potentially leading to larval death. If Hsp90 downregulation upon imidacloprid exposure is a common response, the genetic background may prove to be an important factor in determining the fate of a bee colony. Inbred populations of fruit flies, for example, with slightly decreased Hsp90 expression levels are less fecund and shorter-lived than populations with normal Hsp90 levels [54]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068191#pone.0068191-Chen1>. Together, our finding of reduced Hsp90 expression implies that imidacloprid-exposure affects the developmental buffering system."

I've done some research on the effects of environmental stressors during vertebrate development.  It is a favorite "student research" area of mine, because ambitious undergraduates can be trained within a reasonable period of time to study the effects of their pet environmental toxin on embryo development, and are able, working between classes, to learn many of the basics of "good science" this way.

One of the major effects we see, no matter what insults we offer to the growing embryo, is that if the compound interferes with some developmental pathway, the embryo will divert energy to "solve that problem" at the expense of growth and differentiation.  In plain English, what that means is that treated embryos are too small, and don't mature at the proper rate compared to controls receiving the exact same treatment minus the toxin. Many die before they can reach "birth".  If they do complete embryogenesis, they are usually "runts".  These effects are ubiquitous, meaning that while individual toxins also cause specific problems (for instance, students found that caffeine alters outflow tract development in the heart, while chlorpyrifos causes decreased motor activity), ALL of the toxins also produce smaller, developmentally-delayed embryos with higher mortality rates than the controls.

What we are seeing in this paper is an explanation at the genetic level for reduced growth via diversion of available energy to deal with toxic stress.   The response "unlocks" some normally silent epigenetic variant pathways, and the authors speculate that this is done as a strategy because some of those pathways might be more successful than the "usual" one(s) in overcoming the stress (in this case IMI).  So, we can assume some bees will be born while others just die.  I guess that would probably be seen by the beekeeper as a reduced brood nest/spotty brood, although these authors don't mention whether they saw and/or assessed that.  It does make me wonder if some queens are unfairly disposed of, however.....

There is other evidence that metabolic pathways altered prenatally have lasting effects on the adult organism.  Anyone interested in some published work on the long-term metabolic effects of prenatal stress can google "Thrifty phenotype" for some more reading...it's an area of active investigation.

Another statement that caught my eye was "Functional nAChRs – the molecular target site of neonicotinoids – reside in the plasma membrane as ligand-gated ion channels, composed of five protein-subunits [59]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068191#pone.0068191-Matsuda1>. In vitro studies demonstrate that drug action at nAChRs is influenced by the composition of membrane lipids [58]<http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0068191#pone.0068191-Baenziger1>. Altered abundance of certain membrane lipid species may therefore be a physiological adjustment that counters nAChR-mediated effects of imidacloprid."  I'll be following that one up!  Looks like some interesting reading is ahead.

As a more general comment....it is important to see nature as a continuum from the molecular level right up to the planetary level.  Efforts to separate "field studies" from "lab studies" by valuing one over the other are misguided.  By doing so, one effectively puts on "horse blinders" and then can easily miss the valuable clues that each of these approaches provide, leading us to the next useful hypothesis we should be working on.  It *is* hard work to try and follow all the avenues of research, understand them, separate the wheat from the chaff, and tie the results together.  But, that's what it takes and that's why there are scientists collaborating and communicating, who spend all their working hours trying to figure these things out.

Christina







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