Bradley Woolf
Bradley Woolf
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Genes from the sci-fi book Upgrade
Genes from the sci-fi book Upgrade

Genes from the sci-fi book Upgrade

Upgrade, a book by Blake Crouch, is one of my favorite sci-fi stories. In it, the main characters are shotgun edited by their mother with superhuman abilities. There is a lot of technology to be developed from that book that I would like to work on.

In the book, there are tons of genes that are discussed. I list the ones mentioned below, more for my own reference, but I figured I would share. Most of these are real, but some are made up by Blake to enhance the story.

In my opinion, what counts is not the statistical percentage of one gene affecting some English-described phenotype like eye color or hair color, like what we get with tests like Nucleus and Nebula, but the real molecular biology this gene causes. Understanding this leads to insane engineering ability.

LOF = loss of function, meaning if it doesn’t work, the right side of the arrow (→) is the byproduct

So it goes: gene function → LOF byproduct

SOST: inhibits Wnt signaling in bone → high bone mass

MSTN: negative regulator of muscle growth → large, lean muscles (seen in cattle & rare humans)

SCN9A: Nav1.7 sodium channel → insensitivity to pain

FAAH-OUT: reduced FAAH activity increases endocannabinoids, lowering pain and anxiety

NTRK1: NGF receptor (TrkA) → insensitivity to pain + anhidrosis

HSD17B13: Hepatic lipid metabolism → protection from fatty liver disease

CCR5: HIV coreceptor → HIV resistance

FUT2: Gut epithelial glycosylation → Norovirus resistance

IL23R: Th17 immune signaling → protection from Crohn’s disease

HBB: Hemoglobin β-chain → Malaria resistance

PAH (PKU in book): Phenylalanine metabolism lowers → loss causes toxic phenylalanine accumulation and neurodevelopmental disease

CFTR: Chloride channel → possibly TB/cholera resistance

HEXA: GM2 ganglioside degradation → possible TB resistance (speculative)

PCSK9: LDL receptor degradation → very low LDL, low heart disease risk

GHR/GH/SLC30A8: Growth hormone axis / insulin secretion → diabetes, stature, longevity tradeoffs

IFIH1=MDA5: viral RNA sensing → reduced autoimmunity, altered viral defense

NPC1: cholesterol trafficking → Ebola resistance

ANGPTL3: lipid metabolism regulator → low triglycerides and LDL

EGLN1/EPAS1: oxygen sensing → high-altitude tolerance

MTHFR: folate metabolism → not sure

EPOR: red blood cell production → oxygen delivery changes

BHLHE41=DEC2: sleep duration regulation → natural short sleepers

NPSR1: arousal, anxiety → wakefulness, stress response

ADRB1: Noradrenergic signaling → wakefulness

APOE: ε2 → protective, ε4 → increases Alzheimer’s risk

APP/NGF/NEU1/NGFR: neuronal survival, amyloid processing → heavily drug-targeted, tightly regulated

CTNNB1 (β-catenin): Wnt signaling → cancer is not a simple LOF story; loss breaks development, persistent activation drives oncogenesis

CDKN2A/TP53: tumor suppression → enhancement ≠ trivial; dosage matters (needs better engineering tools)

TERT: Telomerase → longevity or cancer

AAVS1 (PPP1R12C intron 1): safe-harbor integration site on human chromosome 19 for CRISPR knock-in

SHS231: not real

hROSA26: human ROSA26-like safe-harbor locus (less standardized than in mouse, since we have done so much with mice but not a lot with humans)