Scotland end-to-end in 2 days and 6 hours

I’ve been so busy recently I forgot to post an update about my Scotland end-to-end charity cycle! Spoiler alert: I did it. As soon as I got home I moved to the Land of Eng and I’ve been settling in since and never got round to writing a blog post.

To raise funds for the Scottish Association for Mental Health (SAMH), and as a “goodbye for now” to Scotland as I move south of The Wall, I decided to cycle the length of Scotland over 3 days. I trained for it but probably not enough, which is the usual for endurance events. The journey would be just over 400 miles in 3 days. I wanted to do it solo (no other cyclists) and also unsupported (no support car to carry my food etc). I wanted it to be tough. On the 12th of September I got the train up to Thurso and cycled along to John O’Groats. It got dark quickly, became very misty, and a shortcut I thought was a paved road turned out to be off-road in a field (but I did it anyway, on my road bike). Eventually I got to my accommodation, got everything ready for the next day, and slept. It was a great little house hotel with the most wonderful hosts. I met an interesting couple of American ladies who stay there every year and they were kind enough to give me donations. Everyone was going to wake up during the night to see the northern lights but I knew I had my longest day of cycling ahead of me. I went to bed at about 11pm.

The cycling was over the 13th-15th of September. The first day would take me from John o’Groats to Loch Oich (a bit further south than Loch Ness), a good 150 miles. The second day would go from there, passing Fort William and Glencoe, through the Trossachs and along Loch Lomond (where I usually cycle during training), and into Glasgow to call it a day after about 130 miles.  The third day was a coastal cycle as far south as I could get in Scotland. This took me to the area of land south of Kirkmaiden and actually further south than places in England like Carlisle. If I could cycle on water, I wasn’t too far from Northern Ireland. I had to cycle another 20 miles north again to get to the nearest train station then slept in Glasgow another night before coming home on the 16th.

My route on day 1.
My route on day 1, tracked with GPS on Strava.

The most dangerous day was definitely the first. The sea mist was everywhere on the east coast when I was cycling and I couldn’t see more than a few metres in front of my face. If I did this again, I wouldn’t cycle along the coast. When I did see some beautiful scenery that was worth photographing, it was gone before I could get my phone ready. Every picture was mist.

This was how bad it looked when stopped. Imagine cycling nearly 30 mph.
This was how bad it looked when stopped. Imagine cycling nearly 30 mph.
Believe it or not there are mountains behind this wall.
Believe it or not there are mountains behind this wall.

It felt safer when I started to climb and get away from the mist, but the downhill sections were pretty crazy. I didn’t have any accidents on the entire journey but I came close twice and both occurred while flying downhill at nearly 40 mph. Both times I was able to get things under control and avoid an incident. It might not be the Alps, but Scotland has its impressive downhill sections. Ignoring the couple of times I nearly came off, I loved them. Especially after climbing a few thousand feet!

Climbing was the only way to avoid the sea mist.
Climbing was the only way to avoid the sea mist.

The weather improved dramatically as the day went on and I moved further inland. The mist vanished and the sun came out. Food and hydration became my main priority instead of visibility.

Improved weather away from the coast.
Improved weather away from the coast.

I must have passed about 20 whisky distilleries that I noticed. Sadly I didn’t have time to stop at any because I had to cover 150 miles in one day and I didn’t want to be cycling too late into the evening. Firstly, I wanted to avoid cycling in the dark for safety reasons. But I also wanted to be done as early as possible so my muscles could recover for the 130 miles I would be doing the next day.

I didn't have time to stop!
I didn’t have time to stop!

Day 2 started extremely well and I was in a good mood. I cycled strong, I stopped to take pictures where I could. It was exactly how I imagined the ride going when I visualised it during the planning stages. A fun ride through beautiful landscapes. That’s how it started at least.

Day 2 started beautifully.
Day 2 started beautifully.

I’ve been to Loch Ness so many times in my life, but my brain never really gets used to how big it is. This was the first time I had cycled it and it seemed to go on forever. I didn’t mind since the view was constantly beautiful and I was still in a good mood at that point. The only problem was the winding roads and tourist traffic. Many cyclists choose the south side of the loch because it is quieter, but I know the quality of the road is better on the north side and I knew I could cycle it quicker. It was much more dangerous, but I think I made the right decision in the end. The loch is so long that the climate seemed to change while cycling alongside it. At first it reminded me of being back on the coast. I could barely see the other side of the loch for mist. Eventually it cleared and it was a perfect summery day.

The mist on Loch Ness starting to clear.
The mist on Loch Ness starting to clear.
Urquhart Castle.
Urquhart Castle.
Still on Loch Ness, but now everything is crystal clear.
Still on Loch Ness, but now everything is crystal clear.

Everything went downhill after Loch Ness and I’m not talking about gradient. I’d started a little too strong and I was struggling. I cycled for as long as I could, eating small amounts every 15 minutes (while cycling). Eventually I passed a loch (I don’t even know which one) and stopped for a proper meal. On the first day I found it impossible to eat a proper meal because my stomach was in a really weird place having to cope with eating every 15 minutes for a whole day. But this time I ate the entire meal like it was a biscuit, despite my weird regular snacks. In hindsight this was a good idea just to make me feel a bit more normal, but it slowed me down considerably. Not just the stopping for the food, but the meal itself. I was desperately tired and eating a huge meal so quickly just made cycling seem like a really bad idea. I sat for 10 minutes then got back on the bike.

My first break since Loch Ness. Starting to get into trouble.
My first break since Loch Ness. Starting to get into trouble.
A welcome meal to keep me going through.
A welcome meal to keep me going though.

I didn’t stop again or take photos until I got to Spean Bridge. This was a bit of a milestone because at that point I realised I had really cycled from the east to the west of the country. I took another break here and it was the last time on day 2 that I felt good about the ride and the last time I stopped for photos and fun.

Taken from Spean Bridge in the Great Glen.
Taken from Spean Bridge in the Great Glen.
Of course I found time to stop for this one.
Of course I found time to stop for this one.

From here I struggled. I didn’t slow down, I didn’t need to keep taking breaks… actually it was the opposite. I realised that if I took too many breaks they would take their toll. I knew I needed to keep my head down and just keep things steady. Consistent pace, just keep the legs turning. I did take the odd break now and then but just for a few minutes to stretch a bit and write the odd text message. By the time I was getting to Glasgow it was getting really dark as I’d taken too long in the morning and set off a bit later than I meant to. In Glasgow I stayed with my brother and his girlfriend. Their sofa was the most welcome sight and I collapsed.

I’m not going to lie, day 3 was difficult too. Especially at the very end when it was just hills keeping me from my goal. But none of it compared to the day 2. Day 3 was more like the first day. My legs felt warmed up after the previous day cycling and a good long sleep, but I knew not to go too strong this time in the morning. I had over 100 miles to cover but nowhere near as far as the previous days. Most of the day would be navigating my way around motorways and busy roads out of Glasgow and then down the west coast. I tried to keep a good pace because I knew this day was the only one that mattered for my overall time. I was never doing this to set a record, but it has to be said that I couldn’t find a cycling record for this journey anywhere online so I’m happy to set one for people to beat. I knew I couldn’t cycle non-stop like some people have done on the LEJOG route. I needed to sleep at the end of each day, so I knew my ride would take over 2 days even if I was only cycling for less than 20 hours during those 2 days. But on day 3 I could stop the clock once I reached my destination. I wanted to get there asap. There was also the added pressure that I had to cycle another 20 miles back north again to the nearest train station to get back to Glasgow that night. I didn’t want to miss the last train.

Most of the day was a case of keeping my head down and just cycling. I forgot about texting people, I forgot about social media, I didn’t take many pictures except when I stopped to stretch. I just thought about my cadence, calorie intake, and hydration. Once I reached Stranraer I had good feeling for how far was left. I could estimate how quick I needed to be to make the train later. I was tired but suddenly I felt as happy and motivated as I did on the first day. I kept up the pace so I could get a decent time but the hills were constant between Stranraer and the coast south of Kirkmaiden. This was difficult after days of cycling but I enjoyed it. I could feel the end coming up. I had to dodge cows. Every downhill only lasted a moment before I was going uphill again. But it was all worth it as I could feel the entire ride coming to a close and it felt very rewarding. As I reached the last couple of hours of cycling, the clouds rolled in and I thought I was going to see my first rain of the entire journey. Amazingly I didn’t. The sun was gone, the atmosphere completely changed, but it didn’t rain on me once during the entire 3 days of cycling.

The clouds...
The clouds…
...were rolling in.
…were rolling in.
I didn't care if it rained because I knew the end was near.
I didn’t care if it rained because I knew the end was near.
Looking back at some of my cow friends. When I came back down they were all over the road! All of them.
Looking back at some of my cow friends. When I came back down they were all over the road! All of them.

When I finally reached the end of the journey, this was the view I was treated to:

The finish line.
The finish line.

And this is what the most southern point of Scotland looks like:

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Finished! I found a tiny old lady and she managed to take this picture after about 10 attempts. She must have been about 100 years old.
Finished! I found a tiny lady and she managed to take this picture after about 10 attempts. She must have been about 100 years old.

It took me 2 days and 6 hours to cycle mainland Scotland end-to-end. That’s like cycling from Edinburgh to London. It was very rewarding in an athletic sense because I’d never done endurance cycling before. But far more importantly, we managed to raise £1229.53 for the Scottish Association for Mental Health. It’s such a brilliant cause, a genuinely great charity, and I’m so grateful for everyone who donated. I’m also grateful to my friends who weren’t able to donate for whatever reason but gave me support and motivation during training and the ride itself.


I’m sad to have left Scotland and I really do miss it. Sure, it’s only a train journey away, but it’s not quite the same. I’m so glad I was able to take in so much of the country in such a short space of time. It was the perfect way to say goodbye as I managed to see a bit of everything, even if I was struggling to take it all in during the darker moments (especially day 2). I’ve only been back once since I moved but I intend to visit whenever I can. In the meantime I’ll be sipping whisky and listening to Caledonia ;)

Cycling Scotland end-to-end over 3 days

On Saturday I’ll be starting the first of three days cycling the length of Scotland. It’s something I’ve always wanted to do and will serve as a “goodbye for now” as I move to the Land of Eng later in the month. The primary reason I’m doing this is to raise funds for a great charity, the Scottish Association for Mental Health (SAMH). They provide great support for those in need and also tackle the stigma of mental health. One in four people in the UK have to deal with mental health problems.

Various Scottish poems have mentioned the journey from John o’Groats to Kirkmaiden, which is generally considered to be the end-to-end journey for mainland Scotland. Robert Burns wrote of the journey “frae Maidenkirk tae Johnnie Groats” in his poem On the Late Captain Grose’s Peregrinations Through Scotland. Robert Louis Stevenson wrote:

But maistly thee, the bluid o’ Scots,
Frae Maidenkirk to John o’ Grots,
The king o’ drinks, as I conceive it,
Talisker, Isla, or Glenlivet!

The Maidenkirk they speak of is now Kirkmaiden. Although being in Scotland, it’s actually further south than Carlisle. Day 1: Leaving John o’Groats and cycling 160 miles through Inverness, along Loch Ness, and staying the night near Loch Oich. Day 2: Cycling through Fort William, through the Trossachs and Loch Lomond National Park, then on to Glasgow to stay the night. Day 3: Cycling as far south as I can get until I’m pretty close to Northern Ireland! I’ll post an update after the cycle with photos if possible.

If you would like to support SAMH you can donate on my Justgiving page for the ride. Thank you!


I’ve been having a discussion where the term “homology” was thrown around very loosely by someone who should probably know better. Considering deep homology and gene co-option are among my favourite topics in biology, I obviously could feel a rant coming on. Rants are often transformed into blogs these days. Those who have at least heard of the word might think it has something do with things being similar. Those with an interest in biology, especially evolutionary biology, probably realise it’s more complicated than superficial similarity. Sadly, I see the word used in various ways all the time and thought I’d share some thoughts. The word “homology” has been used for over 150 years and has meant different things to different biologists, with similarity of characters being the common theme. Most modern biologists use the word to refer to similarity that is due to common ancestry: two characters are homologous if they are derived from the same ancestral character in their most recent common ancestor. Any characters that exist in related lineages can be assessed for homology, including genes, chromosomes, genomes, cells, limbs, regions of the brain, behaviours, and the developmental programmes that result in these characters. Ancestors are rarely available for examination so homology is usually an evolutionary hypothesis rather than a direct observation.

Even among biologists, the correct definition of homology is still occasionally an issue. Some researchers write of “functional homology” when describing similar functions of traits. Some examples of supposed “functional homology” will be truly homologous in the sense of common ancestry, while others will be non-homologous but convergently similar. In some of the literature, homology still refers to characters that are merely similar, regardless of ancestry. If homology is defined by similarities, there may be a gradient of homology for any given character. Some characters are presumably more similar than others. If they are a slightly similar, are they only slightly homologous? If they are very similar, are they very homologous? Where do we draw the line? When do two similar traits become similar enough to warrant being described as homologous? This subjective issue is avoided entirely when common ancestry is used to define homology. We may not know for certain if two characters are homologous, but they either are or aren’t. This approach makes the concept of homology simpler to define and have researchers agree upon, but requires rigorous investigation to determine if homology exists in any given character.

Homology versus Homoplasy: Image taken from Hall (2003). This image demonstrates the homologous and homoplastic relationships of a character, C. B represents the plesiomorphic state of the character. The Cs in clade 1 are homologous because C already existed in the most recent common ancestor of the two lineages. The same situation is observed in clade 2. But when comparing Cs between clades 1 and 2, the relationship is homoplastic as C did not exist in the most recent common ancestor (3). Lineages 1 and 2 independently evolved the C character from the ancestral B character.

Understanding ancestral relationships in any kind of comparative biology usually involves recognising the differences between homology and homoplasy (as in the figure above). Homology is similarity because of common descent and ancestry. Homoplasy is similarity because of independent convergent evolution. Definitions must be clear. Some related characters are orthologues, arising from lineages splitting and diverging. Others are paralogues, arising from gene duplication. Some genes can also be xenologues if they have arisen from horizontal gene transfer. Understanding homology is essential in comparative biology because of the practical applications of such knowledge. Homology can be used in constructing character matrices for phylogenetic analyses. Also, finding functionally equivalent orthologues of human genes in model organisms has an important role in medical research. A geneticist studying fly orthologues of our genes needs to be sure that he/she has the correct homologue. The same can be said for a medical researcher studying human orthologues in mice that may influence the likelihood of getting cancer or Alzheimer’s disease. It is vital that evolutionary biologists understand what is truly homologous.

One level of homology is that of genes. When genes are replicated, their daughters can undergo independent evolutionary change much like individual organisms can. Phylogenetic analysis is as possible on individual genes as it is on species. Because genes can replicate, either within the same genome (paralogy) or because of a speciation event (orthology), divergent genes can evolve independently but they are homologous due to their common ancestry. Homology doesn’t only occur at the level of genes. Over generations, phenotypes can change considerably. Morphological characters in different species are homologous if they arose from an ancestral state. They may be highly derived and superficially unrecognisable as homologues, they may even have novel functions, but the modern definition of homology is concerned with their relationship with one another rather than superficial or functional similarity. After agreeing on the concept of homology by common ancestry, it’s a relatively simple concept to understand when considering a single level, e.g. a morphological character or a gene. Homology is simply the continuation of characters. The complications arise when the genetic and morphological levels of homology are integrated. Developmental genetics involves understanding the relationship between morphological characters and their genetic basis.

The modern evolutionary synthesis reconciled genetics and the evolution of morphology (and other phenotypic traits such as physiology, behaviour etc) by natural selection. But before the influence of modern evo-devo, developmental was relatively poorly understood compared to traditional genetics and was seen as a black box that transforms the genetic information into three-dimensional, morphological structures. In the last two decades, evo-devo has replaced this black box development with an appreciation of the mechanisms responsible for generating morphological structures from genetic information. How genes are used in development is as important as what genes are available, and lineage-specific differences can come about due to changes in spatial or temporal expression of genes as well as by the evolution of the genes themselves. Development is complex, often involving many genes influencing the expression of each other, and highlights important information about homology. Developmental mechanisms may be conserved even if complete structures don’t form in some species (rudiments and vestiges) and can differ even for structures that are homologous. This suggests that there is a third level to consider, between genes and morphology (or other characters of the phenotype). Can entire gene regulatory networks be homologous? Does this have implications for the relationship between genes and morphology? How can we identify true homologues if there is a disassociation between the genotype and the phenotype? These are questions I find fascinating.

Disassociation between genotype and phenotype

Wagner argued that homology at the levels of genetics and morphology are similar, as morphological characters are equivalent to genetic loci. Just as there may be different alleles present for a gene in a population, there may be different states for a morphological character. A gene and a morphological character can be duplicated during a speciation event. The gene would be an orthologue. The morphological equivalent would be a bat’s wing and a cat’s anterior legs, which are homologous characters in related species. But duplications can also occur within a species. Gene duplication can create paralogous genes. These genes are certainly homologous and have a common ancestor, but both descendents occur in the same genome. The morphological equivalent would be when morphological characters become repeated, such as teeth or extra limbs.

It is reasonable to expect that the genetics of a morphological character can evolve and thus evolve the morphological character itself. Therefore, if a morphological character has evolved, it must be because the underlying genetics have evolved. When homology is applied to phenotypic characters (e.g. morphological structures, behaviours, modes of communication), those characters existed in the last common ancestor. So both levels can be thought of as equivalents of one another and both are relatively simple to appreciate conceptually. Indeed, it isn’t surprising that similar features persist over evolutionary time and in multiple species (homology), especially if the developmental basis of that feature has also been conserved. It also isn’t surprising that different selection pressures can bring about similar features in organisms that do not share a most recent common ancestor (homoplasy). The more surprising observation is that homologous features can be formed from non-homologous developmental processes, and homologous developmental processes can be found forming non-homologous features. It is the relationship between the two levels that complicates our understanding and makes this such a strange issue.

Thinking at two levels of homology (morphological characters and the genes involved in their development), it appears to be a paradox. It doesn’t make intuitive sense that homologous morphological characters are brought about by the expression of non-homologous genes. It is not difficult to imagine a situation where this paradox causes two biologists to disagree over the supposed homology of a morphological character. If one relied on comparing gene expression between species, and the other relied on bone structure or another morphological feature, the paradox could confuse matters. A careful approach considering multiple lines of evidence is clearly required, but which lines of evidence? Is it as simple as genes vs morphology? The relationship between genotype and phenotype is remarkably complex. Developmental processes can evolve independently yet result in the same phenotypic character. This disassociation between the genotype and phenotype has been referred to as “phenotypic drift” or “developmental system drift”. Such a disassociation through evolution can make the search for homologous characters difficult. It can be easy to mistake morphological characters as being homologous just because homologous genes are involved in their development. Inversely, truly homologous morphological characters may be overlooked if it is realised that their genetic or developmental bases are different. It is also important to remember that genes do not operate in isolation. Researchers must consider networks of genes and the role they play in the development of morphological structures.

Homologous genes and non-homologous phenotypic characters

There are many examples of homologous genes being used in the development of non-homologous phenotypic characters. Most developmental regulatory genes of metazoans are more ancient than their developmental roles are. Homeobox-containing genes predate the origin of metazoans yet are often involved in patterning phenotypic structures that are unique to metazoans. Clearly their roles in development have evolved over time with new roles being gained and old roles being lost in some lineages. The segmentation in Drosophila melanogaster, Schistocerca americana and Aphidius ervi is putatively homologous, yet there are genes essential for segmentation in the fruit fly that play an entirely different role in the locust and wasp. The genes fushi tarazu and even-skipped are pair-rule genes in the fly, which divide gene expression into half-segments of the embryo. In the locust and wasp, these genes are involved in the development of the central nervous system rather than body segmentation.

It is a recurring theme that homologous transcription factors can have different roles in different taxa. Orthologues of distal-less, engrailed, and orthodenticle in echinoderms pattern different morphological features than they do in arthropods and chordates. In arthropods and chordates, distal-less is expressed during limb outgrowth and plays a role in proximodistal patterning, engrailed is involved in neurogenesis in the central nervous system, and orthodenticle has a role in the specification of anterior structures. In most echinoderms, distal-less and orthodenticle are expressed in the podia and engrailed is involved in skeletogenesis. But evolution has altered the expression and roles of these genes even among echinoderms. In the Asteroidea (sea stars), distal-less is expressed in the larval brachiolar arms. In the Echinoidea (sea urchins), engrailed is involved in rudiment invagination. In the Holothuroidea (Sea cucumbers), orthodenticle is expressed in the larval ciliated band. These changes in expression and role correlate with novel morphological features such as brachiolar complex of sea star larva or the sea urchin’s rudiment ectoderm invagination. Pre-existing genes have been co-opted for new roles in echinoderms.

Regulatory genes rarely have one role in a developing organism. The Notch signalling pathway is highly conserved and found in all metazoans. In Drosophila melanogaster, it is used in the development of wings, ommatidia, and bristles. These morphological structures are clearly not homologous, yet their development has common genetic features. Throughout the Metazoa, the Notch pathway can be found in the development of characters as diverse as feathers and T-lymphocytes. True conservation also occurs, such as the Hox genes and their role in patterning the anteroposterior axis in animals as different as fruit flies and humans. But these genes often have multiple roles. Although one role can be highly conserved, often there are divergent unique roles for these genes in different lineages.

Non-homologous genes and homologous phenotypic characters

Instead of homologous genes having roles in producing non-homologous morphologies, some homologous morphological characters are produced by non-homologous genes. Sex-lethal is a master regulatory gene that controls sex determination in Drosophila melanogaster. In other dipterans such Ceratitis capitata and Musca domestica, Sex-lethal exists but isn’t used in sex determination and is expressed during a different stage of development. Phylogenetic analysis suggests that the role in sex determination is the derived condition. Where even-skipped was co-opted to be used in the development of a novel morphological feature, Sxl has become involved in a developmental process that already existed. Sex determination in the Drosophila lineage existed before Sxl.

In most tetrapods, programmed cell death separates digit primordia during embryonic development. This creates interdigital space, allowing the primordia to develop into individual digits. In urodele amphibians, differential growth of the digits separates them, without apoptosis creating interdigital space. As a morphological feature, the digits of urodeles and other tetrapods are homologous. But the developmental processes and the genetics controlling those processes are not homologous. This phenomenon of homologous phenotypes being generated by non-homologous developmental processes is not restricted to adult morphology. In vertebrate embryos, the gastrula stage is considered to be homologous. However, it is found that very different developmental processes produce the gastrula in different vertebrate taxa.

Levels of homology

By revealing that development itself evolves, evo-devo implies that homology should be understood in a hierarchical fashion as there are several levels of homology. Homology at one level might not correspond to homology at other levels. As already discussed, two species may have homologous limbs, but the developmental processes that produce the limb, or the genetic cascades underlying those processes, may be different. For example, formation of the neural crest can occur by delamination or by cavitation, and gastrulation can occur via a blastodisc or a blastopore.

Some researchers have interpreted similar patterns of regulatory gene expression alone as evidence that morphological structures are homologous. This ignores the idea that homology may exist at several levels and it limits the evidence to a single source. Assuming that similar gene expression identifies homologous structures ignores the evolutionary histories of the structures and the regulatory genes. What exactly is homologous in a given example? The genes? Their expression patterns? Their developmental roles? The morphological structures that arise because of them? Because some of these levels can be homologous while others aren’t, mistakes can be made when expression data alone is used to assign homology to structures. At least three levels of homology and homoplasy must be considered: genes, developmental processes, and the resulting phenotypic character.

How can a morphological character (like segmentation) be homologous if different genes are involved? The answer lies in understanding developmental genetics and gene regulatory networks. Developmental processes can create different features in different organisms because they can be co-opted for new roles and old pathways can resurface or remain unexpressed, perhaps to be co-opted in the future. Wagner proposed that the homology of morphological characters is related to the continuity of gene regulatory networks (GRNs) rather than the expression of individual homologous genes. He refers to these networks as “character identity networks” (ChINs) and argues that they are what enables the execution of character-specific developmental programmes. In insect segmentation, more variation is seen in the homologous genes that are further upstream than downstream. Gap genes and pair-rule genes are higher in the segmentation hierarchy yet show more variation than lower genes such as the segment-polarity genes. Only the Diptera possess the gap gene bicoid and not even all members of the Diptera. Other segmented insects use different genes at this level of the segmentation hierarchy. But downstream GRNs are more conserved between taxa. Most if not all insects use engrailed and wingless as segment-polarity genes.

Generalising the insect segmentation data, Wagner argued that it is the most downstream regulatory networks, the ChINs, controlling the development of morphological characters that specifies the identity of the character. If homologous morphological structures are controlled by homologous ChINs, this would explain the paradoxical relationship between morphology and genes. The use of different genes in developmental programmes for homologous morphological characters could be explained by homologous ChINs co-opting different individual genes (or pathways) independently. A kernel is a highly conserved GRN. The term ChIN is instead concerned with GRNs that execute a character-specific developmental programme. Some kernels will be ChINs, but not all, as both terms were created for different reasons. One is concerned with conservation and age, the other with the relationship between the GRN and its ability to program character identity. Homologous ChINs can be very conserved, but can also co-opt different transcription factors in their regulation.

So basically…

The complex evolutionary relationship between genotype and phenotype provides two important messages. Firstly, as useful as gene expression data has been, it isn’t sufficient for diagnosing homologous morphological structures. Notch signalling doesn’t suggest that our T-cells and Drosophila eyes are homologous. Regulatory genes have multiple expression domains and play multiple roles in development. Also, it has been assumed that novel structures require novel genes or at least alleles. But how could new alleles or genes become established in a population before they produce an advantageous phenotype? Developmental genes and their ability to have multiple roles suggests an answer to this question. Genes can already exist in a population as new roles evolve and provide fitness advantages for individuals, and potentially the population, given time. Because developmental genes gain and lose roles, some morphological novelties presumably arise by co-opting pre-existing developmental genes for new roles. The echinoderm morphological novelties mentioned earlier provide a good example. At the same time, it’s important not to consider the disassociation between genotype and phenotype as a hindrance to investigation or as noise that stops us from identifying truly homologous characters. There is a lot to learn from studying homology. This phenomenon provides an opportunity to understand how morphological novelties come about and the role co-option plays.

Beyond any confusion caused by multiple levels of homology, there are other common issues in the literature that quite frankly get on my nerves. The nomenclature of genes often makes it difficult. Dlx-2 in Xenopus is not orthologous with Dlx-2 in zebrafish. This example refers to paralogous genes that duplicated before the divergence that led to Xenopus and zebrafish. Even more confusing is when paralogous genes evolve by duplication in independent lineages. It can be extremely difficult to tell which of the duplicates corresponds to the ancestral gene. The homologous gene may have been lost, leaving only the paralogues. Clearly, relying on just one line of evidence isn’t always sufficient for identifying homology. Another major problem is the notion of “functional homology”, which confuses similarity due to common ancestry with similarity due to functional convergence. The functions of homologous genes can diverge from their original functions, or converge on the functions of unrelated genes. Both of these possibilities could confuse a researcher relying only on gene expression patterns as evidence of homology. Clearly homologous structures and genes can have different functions, so similarity of function is not a valid criterion for identifying homology, yet “functional homology” is still occasionally used in the literature. The solution to these two problems is to constantly consider phylogenetics and evolutionary histories when comparing gene expression data. By reconstructing the gene family in all the species being compared, the timing of gene duplications can be calculated relative to the divergences of the species. This approach should improve the likelihood of identifying true orthologues so that only their gene expression patterns are compared.

A third problem that is more difficult to solve (and happens to be one of my favourite biological topics) is the phenomenon of co-option. As discussed, this can lead to the recruitment of orthologous genes to be expressed in non-homologous structures during development. Arthropods, echinoderms, and chordates express distal-less in the distal region of their appendages during their outgrowth, but the structures themselves aren’t homologous. It has become important to distinguish the difference between homology of genes, developmental mechanisms, and morphological structures or other phenotypic characters. To use homology in comparative biology, researchers should observe that homology can exist at different levels and that true homology concerns the evolutionary histories of characters, rather than any general or functional similarity. This approach to homology should be used consistently in studies, whether studying gene expression, developmental mechanisms, or morphological structures. At least that’s what I think.


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