Good question. And it’s been asked before. Usually this question arises within the context of “What use is a larger genome?” when we consider vast genomes such as the onion compared to our own. Why would an onion need a larger genome than we do? After all, humans seem so much more complex than onions (perhaps an anthropocentric bias, I admit). But truthfully, when it comes to RNA and protein production, I doubt an onion really does “need” a larger genome. Not in the sense that it has comparatively more genes to code for. So why would an onion have so much noncoding DNA? Is it just “junk”? And if it is, why does an onion have so much junk compared to us? Surely as super-awesome brilliant talking hairless apes, we should have WAY more junk than they do!
I suspect that one of the reasons we find this question so baffling is that we’re not asking it right. Rather than ask “Why?” instead we could ask “How?”, which may actually give us more insight into what we’re looking for.
How do genomes get larger?
Expansion, recombination, and insertion. It’s about as simple as that. Repetitive sequences have a tendency towards duplication (although deletion, on average, is more frequent); other repetitive sequences also tend to destabilize the local DNA, mismatching with similar homologous sequences, causing slips, hairpins, and other alternative conformations within the DNA that ultimately can lead to deletions, duplications, and inversions on occasion; and, finally, mobile elements cut or copy and paste themselves into the genome and also have a tendency to destabilize the DNA promoting recombination events. In humans, about half of our genome is a remnant of numerous mobile element insertions.
Why would different species have different patterns of expansions, recombinations, and insertions ultimately leading to very differently-sized genomes?
We’re different. Every genome is unique and has gone through its own unique evolutionary histories. As such, each genome has been placed under slightly different pressures. In addition, different species have often been exposed to different types of mobile elements in the form of horizontal genetic inheritance and therefore, while different species may have very similar exomes, the mobile content of regulatory, intronic, and intergenic regions can vary quite considerably. As an example which I’ve mentioned on SoaC before, humans and other higher order primates have a short interspersed mobile element (SINE) called an “Alu” which is unique to them. If you look at the mouse genome, for instance, while it does house other related SINE’s, it completely lacks Alu mobile elements. Interestingly enough, the Alu element has been identified as a potential causal element of destabilization in approximately 1/3rd of segmental duplications in the human genome [1]. That’s astounding. While those duplications have probably infrequently targeted gene products directly, just think how much of a difference that could feasibly make in the regulation of target genes between human and mouse. It’s probably part of what makes a human a human and a mouse a mouse.
When it comes to the onion, its history is different from that of a human or mouse, not only because it is by nature a plant, but also because it maintains the capacity as a true bulb plant to reproduce both sexually through flowering and asexually via producing “bulbils” or very tiny bulbs (the latter thought to be a technique used in times of hardship). Interestingly, it has been shown that mobile elements, when they are not deleterious, have a tendency to expand in number, sometimes rapidly, through asexual reproduction [2]. Because the onion has both an extremely large genome and has the capacity to reproduce asexually, this may in fact suggest that there was a very rough time in the onion’s evolutionary past which necessitated a prolonged period or periods of asexual reproduction which led to a boom in non-deleterious transposable element number and therefore an expansion in the size of its genome.
This is just a single scenario for the onion and there may be several other explanations which might spring to mind. But the point is: the size of an organism’s genome, while fascinating and unique, is no great mystery. No two genomes are alike. This is true to a minor extent within a species, but even more true between species. And, therefore, each species’ genomes have followed different paths. While scientists and laymen alike have gotten over-used to equating the genome with its exome alone, this is a poor way to envision how different changes have arisen in organisms over time. If we want to understand the exome, it’s vital to understand the history of the genome as a whole, regardless of where we each stand in the debate on “junk DNA”.
Let’s face it, when talking about size, comparing the onion genome to the human genome is like talking apples and oranges. They’re just different. Simple as that.
