Who would make a better scientist?
Or this curious little fellow?
One of the most pervasive human traits is perhaps one of the greatest scourges of mankind — the inability to say "I don't know."
There are some things we know quite well about genetics. Many "molecular traits" are rooted in single genes that are passed on to each generation in classical Mendelian fashion. We have one of each gene from our father, one from our mother. Our sex cells have only one copy of each gene, though, so that our children will have half their DNA from us and half their DNA from their other parent. Each sex cell gets a "random" (sort of) allotment of maternal and paternal versions of its genes, allowing each of us to produce children with lots of variability in their traits.
That simple story, of course, is true, at least in a basic sense, even though we may collect more and more caveats as we learn more. But what else is true?
The next time we catch ourselves in a conversation with a presumed "intellectual inferior" when we are about to say "But that's not how genetics works," we may wish to remind ourselves that unless we've scoured the autoclaves and trash cans of scientific laboratories across the world over the last century for all the failed or confusing experiments that genetics researchers have thrown away, we might not know as much about "how genetics works" as we think we do.
A recent review on epigenetics cited two textbooks on fungal genetics, one from the 1940s and one recent, that referred to the common practice of throwing away experiments that defy our current understandings of the science:
As long ago as 1949, Lindegren, reviewing data on inheritance in Neurospora, said that two thirds of new variants do not show Mendelian segregation and are therefore discarded, and, in their recent review of protein inheritance in fungi, Benkemoun and Saupe (2006) commented: "Many of us working with filamentous fungi know how often bizarre looking sectors or segregates that defy Mendelism appear on our plates. As a number of pioneering fungal geneticists have done in the past, maybe we should have a closer look before putting them in the autoclave" (p. 793). They suggested that some of these "anomalies" may be caused by some form of epigenetic inheritance.The definition of "epigenetic" varies, but if we restrict it to mean modifications to the genome architecture that do not change the DNA sequence, there is even more to the picture than epigenetics.
As I pointed out in part II of this series, our understanding of how the cellular anatomy transmits itself from one generation to the next suggests that much of the information necessary to reproduce this anatomy is not coded in the DNA. To date, we have basically no idea to what extent variation in non-genetic but heritable components of the cell contributes to heritable variation in the traits those cells express. As I pointed out in part III, however, there is evidence that protein-folding can directly contribute to inheritance in fungi.
Molecular Biology of the Cell has, even in older editions, discussed other violations of Mendelian inheritance patterns such as gene conversion. This occurs when enzymes just get rid of one copy of the gene and replace it with a double of the other. For example, they might convert the maternal version to the paternal version or vice versa. Again, much of this was worked out in fungi, but researchers are currently trying to unravel the role that gene conversion may have played in human evolution.
We could conclude that maybe fungi are just weird. But we should remember that it is a lot easier to directly study inheritance in microorganisms because each of their generations passes in the blink of an eye compared to ours.
And when we discovered that DNA was the material that transmitted inheritance, we discovered this in bacteria! Bacteria do not even contain histones. As I pointed out in part IV, researchers assumed for decades that histones were just more or less inert stacking material for DNA, but we now know that they play a major role in gene expression and some researchers believe that there are dozens of proteins that form "histone code reader-writer complexes" that write epigenetic codes into our histone proteins and then interpret them. And it's possible, just possible, that some of this coding is passed on from one generation to the next.
And these histone-less bacteria are weird in their own way. As I noted at the end of part IV, Salmonella has an invertible gene that it flip flops to switch between two different kinds of flagella. Don't like your current motile tail? No problem, just read your genes backwards. Gonorrhea has a library of "gene cassettes" that it moves out of position and into its genetic "tape player" in order to modify its traits and evade our powerful immune systems.
We humans (and many other animals) not only have all of the complexities of fungi, but more. As I pointed out in part V, our intestinal bacteria may add a whole 'nother layer to our inheritance pattern.
How much inheritance will turn out to be "bizarre" and how much will turn out to be good ole' classical Mendelism?
At this point, we don't really know.
What we do know is that what exists in the published literature is not a random sample of all the experiments that have been performed. The quote above suggests that publication bias often begins not with the heavy-handed rejection of a journal editor, but with the researcher who can't explain what she or he is observing and decides to just move on and let the anomalous experiment disappear down the memory hole.
Read more about Chris Masterjohn, PhD, here.