VOL III — 05 — RISOGRAPH

Genetics.

From a 19th-century monk counting peas to a CRISPR pipette in a high school lab. The story of how a four-letter alphabet runs every life on Earth.

P.01 / 16 — Mendel

One monk.
Eight years. 28,000 peas.

Gregor Mendel, an Augustinian friar in Brno, crossed thousands of Pisum sativum plants between 1856 and 1864 and discovered three things that contemporaries failed to grasp:

  • DiscretenessInherited traits don't blend; they segregate.
  • IndependenceDifferent traits assort independently.
  • DominanceSome alleles mask others.

Published 1866 in an obscure Brünn journal. Rediscovered 1900 by de Vries, Correns, and Tschermak — the same year Bateson coined "genetics."

Punnett Square — Aa × Aa

A
a
A
AA
Aa
a
Aa
aa

3 : 1 phenotypic ratio. 1 : 2 : 1 genotypic.

P.02 / 16 — DNA Structure

The double helix.

Watson, Crick, and Wilkins shared the 1962 Nobel for the structure; Rosalind Franklin's Photo 51 had given it away. Two anti-parallel sugar-phosphate strands, paired bases inside, 10.5 bp per turn, ~2 nm wide.

  • A — T2 H-bonds
  • G — C3 H-bonds
  • 5'→3'directionality
  • ~2 mper diploid cell
  • 3.2 Gbphuman genome
  • ~20,000protein-coding genes
AT GC TA CG GC AT TA
P.03 / 16 — Central Dogma

How a gene becomes a protein.

1 — TRANSCRIPTION

RNA polymerase II reads a DNA gene and synthesizes a complementary mRNA. Eukaryotic mRNA is then capped, polyadenylated, and spliced.

2 — TRANSLATION

Ribosome reads mRNA codons (3 nt each). 64 codons → 20 amino acids + stop. tRNAs deliver. Result: a polypeptide.

3 — FOLDING

The peptide chain folds (sometimes with chaperones) into a 3D shape — α-helices, β-sheets, motifs, domains. Function follows form.

The genetic code is universal (with a handful of exceptions): the same codons mean the same amino acids in E. coli, in oak, and in you. Strong evidence for common descent.

P.04 / 16 — The Code

Sixty-four codons, twenty amino acids.

Marshall Nirenberg, Har Gobind Khorana, and Robert Holley cracked the codon table by 1966 (Nobel 1968). Most amino acids are encoded by multiple codons — a redundancy that buffers against mutations at the third position ("wobble").

AUG: methionine, also START. UAA, UAG, UGA: STOP.

33 = 27   ·   43 = 64

The code's redundancy is not random — chemically similar amino acids share similar codons, so single-base errors tend to be conservative.

Sample codons

  • AUGMet (start)
  • UUU / UUCPhe
  • GAA / GAGGlu
  • UGGTrp
  • CCNPro (4 codons)
  • CGN, AGA, AGGArg (6)
  • UAA / UAG / UGASTOP
P.05 / 16 — Chromosomes

46 bundles. 3.2 Gb of DNA.

Each human somatic cell carries 46 chromosomes — 23 pairs, 22 autosomal and one sex pair (XX or XY). Each chromosome is a single, long DNA molecule wound around histones into nucleosomes, then into 30 nm fibers, into loops, into chromatids.

Sex chromosomes evolved from a regular autosome pair ~166 Mya in mammals; the Y has shed most of its content and now carries ~70 protein-coding genes vs. the X's ~800.

  • Chr 1249 Mb · ~2,000 genes
  • Chr 2148 Mb · trisomy → Down syndrome
  • Chr X155 Mb · X-inactivation, Lyonization
  • Chr Y57 Mb · SRY locus
  • mtDNA16.5 kb · maternally inherited
12345 6789 karyotype excerpt — 1 through 9
FIG. 1
CRISPR-Cas9.
CRISPR-Cas9 — the bacterial system repurposed (Doudna, Charpentier 2012, Nobel 2020) as gene-editing tool. Therapeutic applications now FDA-approved.
P.06 / 16 — Genome

What's in the genome.

~1.5%protein-coding
~25%introns/regulators
~50%transposable elements
~20%repeats, structural

For decades the non-coding portion was called "junk DNA"; the ENCODE Project (2012) reported biochemical activity in > 80 % of the genome, though "function" remains contested. Much of the regulatory grammar — enhancers, insulators, lincRNAs — lives there.

Lab pipettes
P.08 / 16 — Epigenetics

Above the genes.

Epigenetics: heritable changes in gene expression that don't alter the DNA sequence. The two main marks:

  • DNA methylation5-methylcytosine, mostly at CpG sites; usually represses transcription.
  • Histone modificationsAcetylation (often activating), methylation (context-dependent), phosphorylation, ubiquitination.

Cellular differentiation is largely epigenetic: a liver cell and a neuron in your body share the same genome but read it differently. Some marks survive mitosis; a small fraction may even pass through meiosis (transgenerational, debated).

Examples

  • X-inactivationOne of two X chromosomes silenced in mammalian females (Xist lncRNA).
  • ImprintingMaternal/paternal copies expressed differently — IGF2, H19.
  • Dutch Hunger Winter1944–45 famine cohort showed altered methylation decades later.
  • CancerAberrant methylation of tumor suppressors silences them.
FIG. 2
Mendel's peas.
Mendel (1822-1884) — the founder of genetics. His pea-plant experiments (1856-1863) established inheritance patterns; the work was rediscovered ~1900.
P.09 / 16 — Mutation

Errors are the engine.

Point

Substitution of one base. Synonymous (silent), missense, or nonsense. ~1 in 10⁹ per base per division after proofreading.

Indel

Insertion or deletion. If not a multiple of 3 in coding region, frame-shift; usually catastrophic.

Structural

Inversions, translocations, duplications, copy-number variants. Important in evolution and in disease (BCR-ABL, Charcot–Marie–Tooth).

A human zygote inherits ~70 de novo mutations relative to the parental genomes — most neutral, a few deleterious, very rarely a beneficial one.

P.10 / 16 — Architects

Who built the field.

Mendel

1822–84 · particulate inheritance.

Morgan

1866–1945 · fly chromosomes; sex-linkage.

Avery

1877–1955 · DNA as transforming principle.

Franklin

1920–58 · X-ray crystallography of DNA.

Watson & Crick

1953 · structure paper.

McClintock

1902–92 · transposons.

Doudna & Charpentier

CRISPR-Cas9 · Nobel 2020.

Mello & Fire

RNA interference · Nobel 2006.

P.11 / 16 — Timeline

From peas to gene drives.

1865

Mendel reads "Experiments on Plant Hybrids" to the Brünn Society.

1869

Friedrich Miescher isolates "nuclein" from white-blood-cell pus.

1900

Mendel rediscovered. Bateson coins "genetics" 1905.

1944

Avery, MacLeod, McCarty: DNA, not protein, is the genetic material.

1953

Watson & Crick model the double helix from Franklin's data.

1966

Genetic code fully decoded.

1977

Sanger sequencing; first viral genome (φX174) read.

1983

PCR — Kary Mullis amplifies DNA in a tube.

1990–2003

Human Genome Project: $3 B, 13 yr, 92 % of euchromatin.

2007

1000 Genomes Project; HapMap completes; GWAS era begins.

2012

Doudna & Charpentier publish CRISPR-Cas9 as a programmable nuclease.

2020

mRNA vaccines deployed against SARS-CoV-2 within 11 months.

2022

T2T consortium completes the gapless human genome (3.055 Gbp).

2024

First base-edit therapy approved for sickle-cell disease (Casgevy).

FIG. 3
Human genome.
The Human Genome Project (1990-2003) — sequenced the ~3 billion base pairs of the human genome. Cost ~$3 billion; today a genome costs <$200.
P.12 / 16 — CRISPR

CRISPR-Cas9.

CRISPR-Cas9 is a programmable molecular scissor. The Cas9 protein, guided by a 20-nt guide RNA you design, cuts DNA at a specific site. The cell repairs it — by error-prone NHEJ (knock-out) or HDR with a template (knock-in).

Originally a bacterial immune system: archived viral DNA (CRISPR repeats) as templates to chop matching invaders. Doudna and Charpentier showed in 2012 it could be retargeted at will. Awarded the 2020 Nobel.

Base editing (Liu, 2016) and prime editing (Liu, 2019) edit without double-strand breaks. They underlie 2024's approved therapies for sickle-cell disease and β-thalassemia.

5' 3' Cas9 guide RNA · 20 nt → blunt double-strand break → NHEJ (knock-out) or HDR (knock-in)
P.13 / 16 — Disease Genetics

What breaks.

Mendelian

Single-gene disorders. ~7,000 known. Sickle-cell (HBB), cystic fibrosis (CFTR), Huntington's (HTT). Highly penetrant; relatively rare.

Polygenic

Hundreds to thousands of variants of small effect. Type 2 diabetes, schizophrenia, height. Polygenic risk scores predict probabilistically.

Somatic / Cancer

Mutations accumulated over a lifetime. Driver vs. passenger. KRAS, TP53, BRCA1/2, EGFR. Tumor genomics now routine.

P.14 / 16 — Ethics

What we should do.

The 2018 birth of CRISPR-edited twins by He Jiankui shocked the field — heritable germline editing in humans had been a self-imposed red line since the 1975 Asilomar conference. He served three years in Chinese prison. The moratorium on germline edits remains in force; somatic edits are progressing rapidly.

Other live debates: gene drives in wild populations; DTC genetic testing privacy; reproductive screening; equitable access to expensive therapies (Casgevy: $2.2 M/dose).

Three lines

  • 1Somatic vs. germline
  • 2Therapy vs. enhancement
  • 3Individual vs. species-level effect

Each line is a moving negotiation between technology, regulation, and values.

P.15 / 16 — Frontier & Open Questions

What's next.

Pangenome

A reference graph that captures structural variation across populations, replacing the linear GRCh38.

In utero editing

Fetal CRISPR for monogenic diseases — animal proof of concept; first human trials approaching.

Synthetic genomes

Yeast Sc2.0 nearly complete; bacterial genome write at the megabase scale routine.

Still open.

P.16 / 16 — Go Deeper

Watch & read.

Veritasium & Kurzgesagt — CRISPR

Kurzgesagt's "Genetic Engineering Will Change Everything Forever – CRISPR" — the field's most-watched explainer.

Watch ↗

References

  • WatsonMolecular Biology of the Gene (8e, 2017)
  • MukherjeeThe Gene (2016)
  • Doudna & SternbergA Crack in Creation (2017)
  • Strachan & ReadHuman Molecular Genetics
  • NHGRIgenome.gov educational pages