#initial mutations

[linkerbell]

Cult of Little Nightmares AU I was cooking a couple weeks ago. 🫢

It’s not fully polished or anything but I felt bad not posting art so I’m sharing early.👍

[keferon]

What if instead of magic being what turned the seal skin a part of drift it was some stuff that mutaded the leviathans/funky chemicals released in the tsunami that then reacted with mer dna that of the seal skin wich after he wore it a while began to what it did.

Just a wierd idea i got

So let's instead of using magic of love and friendship make the whole turning process be very unnatural and creepy and painful is what I'm hearing?

[monsters-demons-and-heralds-ohmy]

We know Machine Herald Viktor's ideas of perfection are flawed and influenced by societal values and personal opinion. We've already talked about Viktor's white and gold puppets representing the Piltovian ideal and the shrine Viktor keeps with puppet Jayce and letting Jayce keep his face scar. But, can we talk about the NEWTS?

Like... The only animals we see bigger than an insect that survived the glorious evolution were NEWTS?

You ain't slick wizard man.

[itsmistyeyedbi]

I don't know how many of the people who play twc have watched Arcane, but I do imagine the scene where Murphy carries out his experiment on the detective to be like the scene where Jinx gets injected with shimmer

[xxplastic-cubexx]

Question: do you think Charles ever used his groovy mutation line on Erik and if so what physical feature did he pick? Perhaps Erik’s big d[GUNSHOT]

For a moment i forgot the Groovy Mutation line is from First Class and i was gonna point out the literal mutation that is erik’s white hair and say that

Tho ig that line could still work in movieverse…. I think….. just blonde hair.. or w/e fassbender’s hair color is Lowkey I Kinda Never Think About It

[thegoldenlily]

If Singed had a daughter once, is she the reason the mutation must survive? Is the mutation a part of her?

[termagax]

elaborating on this before i lose my nerve i just in general think hog is way more turned on by their weird fish person traits than either of them expected and while fish is just kind of confused by all this they just kind of let him do whatever he wants which is how he ends up with eggs in his butt. they didnt even ask him to do that.

[tardis--dreams]

I think learning irish would cure me

[prismit]

couldn't find any documentation on how many cells you get from boss rush, so i worked it out myself! (to the best of my abilities anyway lol, also if this info is out there already then i must have missed it in my search 😅 sorry)

quick note: this might not be 100% accurate, since i mostly used math instead of fighting every boss 6 times lol. but i definitely gathered enough data to find a consistent pattern, so if these numbers are off at all, they should at least be VERY close, and at least 0bc and 5bc are definitely correct.

so, here's the numbers for each difficulty!

Concierge: 24 / 25 / 26 / 27 / 28 / 30

Conjunctivius: 40 / 42 / 44 / 46 / 48 / 50

Mama Tick: 32 / 33 / 35 / 36 / 38 / 40

Death: 80 / 84 / 88 / 92 / 96 / 100

Time Keeper: 40 / 42 / 44 / 46 / 48 / 50

Giant: 60 / 63 / 66 / 69 / 72 / 75

Scarecrow: 50 / 52 / 55 / 57 / 60 / 62

Dracula: 80 / 84 / 88 / 92 / 96 / 100

Hand of the King: 80 / 84 / 88 / 92 / 96 / 100

Servants: 47 / 49 / 51 / 54 / 56 / 60

Queen: 80 / 84 / 88 / 92 / 96 / 100

Dracula Final Form: 40 on all difficulties

ALSO: you don't get any more cells than normal from modified bosses or flawless wins. the 4 trials give the same amount as DIY mode, so there's no bonus there as far as cells go.

[highlifeboat]

Honestly, I got invested only because I got obsessed with idea of writing fanfic with premise:

"A girl doomed by narrative fucking claws and bites her way against literal God of the forest, to get her happy ending (In the process fucking up everyone around her even more than they already were)" :p

I dig that for a premise tbh.

I wish this show was more like that.

Just a bunch of girls in the forest slowly losing their humanity as they try to survive circumstances beyond their control.

I like that kind of idea. (But I would be adding shit like forest creatures and a happy ending that isn't really happy)

[ourtlesofturtles]

Mondo Gecko! Wow what a cool dude

-

here’s Slash and Leatherhead as well :)

[frost-sama-senpai-san]

He wanted to turn ALL the big anti mutant supporters into mutants!

[fourgottencoast]

wrt covid if i had to choose i would much rather people wear n95/kn95 masks than get vaxxed considering we STILL don't have a sterilizing vaccine that prevents transmission and infection- masking and cleaning the air are currently the only preventative measures :/ (and while they may not be 100% effective the less viral load you intake and the less infections you get overall, the better)

[townpostin]

Seraikela Land Office Clerk Arrested in Bribery Sting

Anti-Corruption Bureau Nabs Official Accepting ₹8000 for File Processing A head clerk at Land Reforms Sub-Collector’s Ofice caught red-handed in ACB operation following complaint from local landowner. SERAIKELA – The Anti-Corruption Bureau (ACB) has arrested S Nanda, a head clerk at the Land Reforms Sub-Collector Office in Seraikela, for allegedly accepting a bribe of ₹8000. The arrest occurred…

[horsesarecreatures]

Horses are among the world’s most elite athletes: When galloping, they can consume twice as much oxygen per kilogram as the fittest humans. All that oxygen supercharges horses’ cells’ energy-producing compartments as they crank out ATP, the chemical needed to power their impressive muscles. But making so much cellular fuel so quickly comes with a catch: the manufacture of pernicious byproduct molecules called reactive oxygen species (ROS), which can wreak havoc in cells.

How horses dealt with this biological trade-off and evolved into premier endurance athletes has long intrigued biologists. Researchers report today in Science that they have uncovered a big part of it, identifying a key mutation that lets horses safely produce so much ATP. The trait helped pave the way for horses to go from dog-size critters millions of years ago to the high-endurance athletes we know today.

The study’s detailed molecular work makes it “exceptional,” says José Calbet, an expert on the cellular responses to exercise at the University of Las Palmas de Gran Canaria who wasn’t involved with the study.

The mutation in question occurs in the gene that encodes a protein called KEAP1, which acts as a biochemical bouncer, binding to a different protein called NRF2 to prevent it from entering the cell’s nucleus, where it would otherwise activate stress-response genes that help blunt cell damage.

But ROS can help NRF2 sneak in by causing KEAP1 to release its bind on the protein, allowing it to enter the nucleus and trigger the cell’s stress-response genes.

Johns Hopkins University ophthalmologist and clinician scientist Elia Duh, a senior author of the new study, didn’t set out to study horses. Initially, Duh was interested in the KEAP1-NRF2 system because its role in activating stress-response genes makes it a tempting target for treating inflammation—and aging-related conditions, such as blinding retinal diseases, irritable bowel syndrome, and neurodegeneration.

Duh wondered whether any insights could be gleaned from studying the evolution of these proteins in different animals. So, he teamed up with Gianni Castiglione, an evolutionary biologist and biochemist at Vanderbilt University. Together, they scanned hundreds of vertebrate genomes looking for notable mutations to the gene for KEAP1.

The team’s genomic work revealed birds had almost completely lost the gene, presumably an adaptation to the extreme demands of flight. When they looked in horses, researchers noticed what initially appeared to be a DNA sequence that encoded an unusually short—and therefore presumably nonfunctional—version of the KEAP1 protein. But when Duh’s and Castiglione’s team grew horse cells in culture, it discovered the protein was very much there and working. “Naturally, I was worried I was doing something wrong,” Castiglione says. “Then one day, a light bulb went off.”

As it turns out, the computer algorithm scientists had used to scan the horse genome had made a mistake. The algorithm had spotted a specific kind of mutation in the part of the KEAP1 gene that changed the messenger RNA from CGA—which codes for the amino acid arginine—to UGA, which is what’s known as a “stop codon.”

Normally, the cellular machinery interprets UGA as a sign to stop translating the RNA into a protein. But instead, the horses’ genetic machinery recodes the stop codon into a different amino acid, cysteine, causing it to ignore that order. This phenomenon, known as a stop codon read-through, is common among viruses but rare in multicellular organisms.

“The identification of this evolutionarily significant UGA recoding event represents a potentially seminal finding, offering a model for uncovering other yet-unidentified cases of stop codon read-through,” says Hozumi Motohashi, a biologist at Tohoku University who has studied KEAP1 and NRF2.

That the replacement is a cysteine is particularly notable, Castiglione says. KEAP1 senses cellular stress through its cysteines, which contain sulfur atoms whose reactions with ROS, induce the chemical changes that cause KEAP1 to let go of NRF2. The mutation the researchers had identified adds another place on KEAP1 for ROS to interact, which makes the protein more sensitive to stress—and lets horse cells respond much faster to the cellular stress of intense exercise. “It does make complete sense [that] by introducing another cysteine, another sulfur, you would have heightened sensitivity,” Castiglione says.

What’s more, this tweaking of KEAP1 is a “[key] genetic component to the puzzle of the evolution of horses,” Duh says. “Once they figured out how to run, they could occupy all kinds of ecological niches,” Castiglione adds.

The finding could also point the way toward new kinds of drugs to treat diseases by targeting the specific parts of the KEAP1 protein that help horses hoof it. “By looking at what evolution has figured out, we know this is a viable strategy,” Castiglione says.

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