Know Thy Enemy (Part 2): Inbreeding & Varroa Mites 


Female varroa mite under a dissecting microscope.

Author: Heather Broccard-Bell, Ph.D., Honey Bee Health Researcher. Featured photo credit: H. Broccard-Bell.

 

Know Thy Enemy (Part 2): Inbreeding & Varroa Mites

NERD ALERT: Our blog series on Understanding Varroa is meant to give those that are interested an understanding of what is currently known about varroa mites. At times, this means we’ll be taking detours into some deeper scientific topics. I recognize this will not be everyone’s cup of tea! Don’t worry – we’ll be getting back to some more practical posts soon. In the meantime, you can always check out our previous posts on topics like feeding, wrapping, etc.


Any time the strange lifestyle of varroa is discussed, I hear beekeepers ask about inbreeding. As we learned in Part 1: Who is Varroa Destructor?, varroa reproduction often involves matings between sisters and brothers, and between mothers and sons. To us, such an arrangement sounds distasteful, to say the least.  

Many organisms have developed mechanisms to avoid inbreeding, strongly suggesting that inbreeding is undesirable for reasons deeper than simply offending our human social sensibilities. So, why do varroa seem to be an exception? In this post, I will explore the answer to this question and reveal a couple of ways we have learned that varroa are able to avoid the pitfalls of inbreeding. Along the way, I’ll also touch on some related topics, including how varroa become resistant to the chemicals some beekeepers use to control them. 

Understanding the Problem with Inbreeding 

 To get the full picture, we’ll need to dive into a bit of genetics and look beyond bees and varroa. Ultimately, the reason that inbreeding is so bad boils down to how it limits genetic variability. But what is genetic variability, and why do organisms need it anyway? Throughout this post, I am going to occasionally use dice rolling (the kind found at a casino) to explain how genetic variability works.   

First, let’s briefly shift our focus to the world of the very, very small. Most of the life on our planet is invisible to us and almost all microscopic life consists of organisms, like bacteria, that are each only single cells. Single-celled bacteria reproduce by dividing into two identical daughter cells. Genes – the blueprints for life stored in molecules of DNA that exist in all living cells — are copied before the cell splits, so the daughter cells have identical genes to the parent cell. Except when they don’t, that is. 

Because genes can change. Like mistakes made while taking notes, errors can happen any time genes get copied. Copying errors – what we call mutations — then get inherited by all descendants of the organism. The result is that some members of the species will have one version of a gene, while others have a slightly different version. 

But aren’t mutations bad, you might be asking? While it is certainly true that mutations can be harmful, such as when they produce cancers that kill organisms, they don’t have to be. In fact, small mutations often have no effect at all, since slightly different versions of the genetic blueprint often produce the same end product. And in rare instances, a copying error results in a new genetic blueprint that builds a better version of the organism.   

Diversity is the Engine of Life  

Most bacteria reproduce very quickly, generating populations in the millions from a single parent cell in a matter of hours. We can think of bacteria dividing like rolling dice: the more times the dice are rolled, the more likely it is that you’ll roll a “winning” combination. Similarly, the more times genes are copied, the more chances there are for copying errors, or mutations. Bacteria that have harmful mutations mostly die before they can pass on their specific mutations to daughter cells, whereas bacteria with neutral, or no mutations carry on as usual.  

But for the lucky individuals that have mutations that make them slightly “better” than their counterparts, they will gradually replace the “original” version of the bacteria. What it means to be slightly better can be almost countless number of different things, depending on what specific qualities are advantageous for the bacteria in that environment. For example, if a species has access to a large amount of sugar, the ability to eat sugar would be a useful mutation, making an individual “better” than others that lack this capability. But if these organisms were in an environment with no sugar, a new sugar-eating mutation would not be helpful. Good, bad, and neutral are relative terms when it comes to mutations. 

 

The ability for genes to mutate is a feature, not a bug. Without mutations, living things would not be able to deal with change—and the only thing constant in the world is change! 

 

If we imagine a species whose genes are always copied perfectly during reproduction, every member will have exactly the same genes. Identical genes means the same strengths, but also the same weaknesses. Any significant environmental shift – for example, a large change in temperature — would mean game over for everyone.  

The ability for genes to mutate doesn’t automatically guarantee a species will survive change, because just the right mutation needs to occur to deal with the specific type of change. However, just like dice rolling, there is no chance of winning if you don’t play at all.  

Resistance: Genetic Dice Rolling in Action 

The bacteria story above might sound familiar to some of you, since it’s the same principle driving varroa’s ability to develop resistance to the varroacidal chemicals we use to treat our honey bee colonies. When varroa reproduce, random gene mutations can cause individuals to occasionally be born with the ability to resist the toxic effects of these chemicals.  

A varroa mite with the toxin-evading ability could survive a chemical varroa treatment—and go on to have offspring that have the same ability—while those lacking the ability neither survive nor reproduce. Soon, the entire population of varroa in that area has the mutation that makes them able to resist said toxin, and this treatment stops working. 

Uncovering how resistance arises also helps us to understand why varroa tend to develop resistance to certain types of chemicals but not others. Some varroacides kill varroa by affecting only one kind receptor on the surface of cells within the body. For such chemicals, a single random mutation is often sufficient to allow the varroa to get around the chemical’s effects. Organic acids, like the formic acid in Formic Pro and MAQS, have a much wider range of damaging effects on varroa. This means it’s quite unlikely varroa will become resistant to formic acid treatments, since a lot of different mutations would be required to occur all at once.  

A New Way to Play: Genetic Variation through Sexual Reproduction 

In species like varroa, reproduction happens much more slowly than it does in bacteria. Mutations still occur as individual cells (and their genes) divide the same way as in single-celled organisms. However, passing on mutations doesn’t happen nearly as quickly, which makes varroa’s adaptation to changing environments a longer process.  

Earlier I mentioned that random copying errors mean that some organisms will have one version of a gene, while others will have a slightly different version. Most organisms that reproduce using sexual reproduction, including humans and varroa, end up with two different sets of genes: one from our mothers and one from our fathers*. Different versions of genes can do different things – but it also turns out that different combinations of these gene versions can also have different effects. 

 

Slowly-reproducing organisms like humans and varroa have gotten around the problem of not being able to roll the genetic mutation dice as often by coming up with a different way to roll the dice: sexual reproduction.  

 

Varroa and Inbreeding 

How does this all relate to varroa and inbreeding? Inbreeding decreases the ability of sexual reproduction to shuffle around different versions of genes, since closely-related organisms have more of the same versions of genes than those that are more distantly related.  

When closely-related organisms reproduce, their offspring will have a smaller number of possible genetic combinations – that is, a smaller number of “dice rolls”. The fact that varroa have developed resistance rather quickly to a number of the chemicals we use to control them suggests that the story of their reproduction is not fully captured by the standard narrative.  

A More Nuanced Inbreeding Story 

Typically, a single mated varroa female “foundress” occupies a single capped honey bee brood cell, so any female offspring she produces has no choice but to mate with their brother. However, when mite loads are high, multiple foundress mites can invade the same brood cell. With multiple mite families mingling in one cell, sons can mate with the daughters of different mothers—what scientists call genetic diversity through vertical transmission. We’ve learned that when females mate with unrelated males, they go on to produce more offspring than females that mate with their brothers.  

Evidence has also emerged suggesting much more drift of bees occurs between colonies than was previously suspected. Thus, mites that are genetically different can arrive from different colonies—what scientists call genetic diversity through horizontal transmission. When a group of organisms stays in one place for a long time, they tend to become more genetically similar to one another—kind of like stirring a can of paint. Initially, there might be distinct colours, but as you keep mixing, everything inside the can starts to look the same. But add paint from two different cans together, and you have multiple colours once again. 

Inbreeding is The Price of Parasitism 

Part of the answer to the inbreeding question is that varroa just aren’t as inbred as we originally thought. But the fact remains that they are substantially more inbred than a lot of other organisms. For varroa, inbreeding seems to be a price they had to pay for the opportunity to feed on honey bees and to survive within honey bee colonies.  

In order to avoid being removed or killed by honey bee workers during their vulnerable reproductive phase, varroa had little choice but to begin reproducing under the sealed brood cap, where inbreeding was inevitable. The ability to survive outweighed the hit varroa took to genetic diversity. However, the behaviours discussed above that promote genetic diversity suggest that strong pressure to increase genetic diversity continues to exist, even in varroa.  


I hope I have managed to shed some light on this intriguing and complicated topic. And I hope you’ll join me for my next post in this series, during which I’ll discuss some of the wholly alien abilities varroa have that allow them to lead their bizarre lives in such close proximity to our honey bee friends.
 

 

FOOTNOTE 

* As I outlined in Part I of this series, male varroa, like male bees, develop from unfertilized eggs. Consequently, males, unlike females, have only 1 set of genes. The genetic diversity narrative gets a little murkier here, but essentially, since the males get a randomly-generated subset of the genes from their mother, the opportunity to shuffle sets of versions of genes around still exists. On top of the different combinations of gene versions being able to produce different effects as I discussed in the text, wholly different genes can also interact with one another – a phenomenon called epistasis. 

By the way, scientists’ knowledge of genetics is rapidly changing, and the story is vastly more complicated than what I’ve presented here. Indeed, the story itself is much larger than just genes. Suffice to say that during my teaching career before I started working for NOD, I taught the same genetics course a couple of years apart. From the first teaching to the second teaching, so many new discoveries were made that I had to re-do whole sections! 

 

About Heather Broccard-Bell, Ph.D.

Dr. Heather Broccard-Bell is the Honey Bee Health Researcher at NOD Apiary Products. She is a scientist and educator with over 15 years research and teaching experience. Heather has been focused on investigating issues surrounding honey bee health and communication since 2014. When Heather’s not in the lab, you can usually find her in the bee yard or on a trail hiking with her many pawed pals. If you’d like to ask Dr. Heather Broccard-Bell more about her work or this article, you can email her at heatherb@nodglobal.com 

 

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