Reviving parts of Discover Albia that went quiet awhile ago has been the theme as of late! This time we can take a look at a new case study, which hasn’t happen in ages. A very special thanks to Wolpertinger for submitting not one, but two Norns! The genetics in Creatures 1 are rather simple, while C3/DS genomes contain much more complicated genes. This proved to be the perfect opportunity for me to challenge myself to figure out a little bit more! And as always, if you have something to add or want to suggest a better explanation, comment away! I consider these case studies to be learning experiences for everyone. Maybe you’ll learn something, or have something new to teach me!
These two boys, named Atalo and Atalos, were identical in appearance. I was glad to use Amaikokonut’s Creatures Nametags to help me tell them apart! Wolpertinger explained that Atalo was still a baby at nearly 3 hours old, constantly complained about being intensely hungry for starch even with a low drive, had difficulty waking up on his own, and had experienced almost entire organ death. Additionally, his hunger for protein spiked when he was slapped by the hand, and his boredom spiked when slapped by a Creature. I knew there was quite a lot cooking in his genome from this description! So much to investigate…
I took a moment to look at Atalos, since the two were from the same world and likely shared similar ancestors. Luckily, they were actually much more similar than I expected! So I decided to jump into a double case study and look at them together. There are some big differences between them, yet it isn’t like I was looking at a Norn vs. a Grendel! Wolpertinger reported that Atalos was also stuck in his life stage, never slept, complained about his hunger while staring at food, and constantly looked sad. More mysterious mutations to look into! These little details really helped me out, though, since I at least had an inkling of where to start.
Normally I jump right into a huge discussion about genetic differences, but we just went through a lengthy analysis of some genome changes. I’m also aware that staring at genetic explanations can be a little daunting. What to do? I imported both little guys to verify what was going on and to see if I could get any other ideas about where their mutations might be in their genomes. This is a great way to start your own case study, too! Observation plays a key role. Just finding the mutations within the Genetics Kit doesn’t mean that they’ll have any effects: Some mutations look major, and then it turns out that they do nothing.
The Hoverdoc confirmed that Atalo was intensely hungry for starch, even though I watched him eat several types of food. I also used the X-ray agent to take a look at Atalo’s organs. Sure enough, nearly all of them were completely dead. This one was a little unnerving because I haven’t explored how C3/DS organs work in detail. So I dove into a genetic analysis to see what I could find. And find I did! I took several pages of notes, simply marking where the differences existed. Atalo seemed to have more going on in the mutations department than Atalos, although they were both filled with unique genes! Some were good… Others were a little alarming.
The two boys looked remotely interested in their time in the spotlight! I had no idea what Atalos was really thinking with his sad face, but Atalo looked pretty excited. Or maybe he was running away from the robin that looked like it was chasing him! To avoid getting too bogged down with a ton of information, I’m only tackling one type of gene in this introduction to the case study. The real “meat” of the genetic breakdown will come in one or two additional parts. There won’t be too long of a wait, though! We’ll mainly be looking at receptors, emitters, reactions, stimuli, and instincts. Onto a somewhat short analysis of the mutations in their chemical reactions!
Chemical reactions define rules for individual chemicals and chemical combinations. These genes can also state the rules for how chemicals are used up, and each reaction has a defined half-life to determine how often it occurs.
Original: 251 Emb B MutDupCut Organ# = 14, 1*Sleepiness backup + 1*Sleepase => 1*Sleepiness + 1*Sleepase; half-life = 7
Mutation: 251 Emb B MutDupCut Organ# = 14, 1*Sleepiness backup + 1*Sleepase => 1*Tiredness + 1*Sleepase; half-life = 7
This gene defines the way sleepiness backup is converted into sleepiness. My understanding is that any backup chemicals are generated when a drive is less important than another priority. So if a Norn is being attacked, sleepiness is ignored until a later time. For both Atalo and Atalos, this gene is quite broken! Sleepiness backup is converted into tiredness, which can also be understood as exhaustion. I usually use the exercise example to think about tiredness vs. sleepiness: If you wake up fully refreshed in the morning and do an intense workout, you’ll feel tired afterwards, but most likely you won’t feel like you want to go back to sleep. This mutation might explain why the two Norns tire out more easily, yet it doesn’t address any of the original concerns. Not a terrible mutation by any means, though!
Original: 419 Emb B MutDupCut Organ# = 19, 1*Amino Acid + 1*Fatty Acid => 2*Prostaglandin; half-life = 31
Mutation: 419 Chi B MutDupCut Organ# = 19, 1*Amino Acid + 1*Fatty Acid => 2*Prostaglandin; half-life = 31
For reference, the organ affected is the bone system… Which might not seem like an organ, but that’s just how things work. This gene defines the reaction that produces prostaglandin, which is the chemical responsible for healing injuries. Norns are designed to go through some wear-and-tear throughout their lives. Things like falling from ledges, being slapped too many times, or fighting off an infection all contribute to injuries. The mutation means that this gene only switches on in childhood, which is actually quite dangerous. Organs are highly susceptible to injury during the baby life stage. This might not be much of a problem… Except for Atalo, who is stuck as a baby. Although we haven’t looked at every gene yet, my guess is that this is the main (or sole) reason that all of his organs are dead. There is a separate gene that is keeping Atalo in his first life stage, and this is a perfect example of how two separate, relatively minor mutations can work together to create a bad situation. Atalos suffers from the same mutation, yet his organs are in decent shape because he is a child. Don’t worry: Atalos has his own problems to worry about!
New: 823 Emb B MutDupCut Organ# = 21, 5*CA smell 5 (water) => 1*Fear; half-life = 32
Rather than a mutation, this gene is entirely new when compared with the CFE genome. My feeling is that it was intentionally added at some point. It converts the “smell” of water into fear, thereby creating Norns who tend to stay away from bodies of water. This is a useful gene because it deters accidental drowning. So even if it is some sort of mutation or copied gene, Atalo and Atalos have a less chance of drowning.
Original: 224 You F MutDupCut Organ# = 12, 1*Oestrogen + 1*Progesterone => 1*Progesterone; half-life = 0
Original: 224 Ado F MutDupCut Organ# = 12, 1*Oestrogen + 1*Progesterone => 1*Progesterone; half-life = 0
First, this is a gene that only affects females. Second, only the life stage mutated… And Atalo will never advance beyond being a baby. I think it’s safe to say that this will have absolutely no effect!
Original: 343 Emb B MutDupCut Organ# = 18, 1*Glycotoxin + 1*Arnica => 1*; half-life = 31
Mutation: 343 Emb B MutDupCut Organ# = 18, 1*Sleep toxin + 1*Arnica => 1*; half-life = 31
Glycotoxin poisoning can be deadly, but it can be cured with arnica. That is, that works in the standard genome. For Atalo, this is a rather unfortunate mutation. Arnica no longer cures glycotoxin poisoning. Instead, it removes sleep toxin from his system. On one hand, this means that sleep toxin can actually exit his system in this unique way. This could be a deadly tradeoff, though, since he can’t be cured of glycotoxin. It isn’t always fatal, yet Atalo will get no relief from the typical arnica cure. Let’s just hope he never encounters glycotoxin in his lifetime.
Original: 344 Emb B MutDupCut Organ# = 18, 1*Heavy metals + 1*EDTA => 1*; half-life = 32
Mutation: 344 Emb B MutDupCut Organ# = 18, 1*Cyanide + 1*EDTA => 1*; half-life = 32
Perhaps fate intervened to give Atalos a similar mutation to Atalo’s last one related to glycotoxin and arnica! This gene acts in practically the same way: EDTA normally acts as the cure for heavy metals. In Atalos, it works to remove cyanide from his system. It’s a double-edged sword: He has a little extra safety in place to avoid fatal cyanide poisoning, but heavy metals can never be cured. If I’m correct, poisoning from heavy metals is more common near the Creatures 2 volcano, and C3/DS Norns don’t normally come in contact with the chemical. So this might be a slightly advantageous gene for Atalos, although I would still mark it as a potentially fatal mutation.
That’s it for now! Not too bad, right? There are plenty of other genes and mutations to explore as we dig further into this double case study. Atalo and Atalos will be back soon to show off their genomes. Thanks again to Wolpertinger for sending them in and giving me the chance to explore Creatures Docking Station genetics in more detail!