Slow Death The death cap mushroom, Amanita phalloides,...

Slow Death The death cap mushroom, Amanita phalloides, contains several dangerous substances, including the lethal $a$ -amanitin. This toxin blocks RNA elongation in consumers of the mushroom by binding to eukaryotic RNA polymerase II with very high affinity; it is deadly in concentrations as low as $10^{-8} \mathrm{M}$. The initial reaction to ingestion of the mushroom is gastrointestinal distress (caused by some of the other toxins). These symptoms disappear, but about 48 hours later, the mushroom-eater dies, usually from liver dysfunction. Speculate on why it takes this long for $\alpha$ -amanitin to kill.

Labs

Want to see this concept in action?

NEW

Explore this concept interactively to see how it behaves as you change inputs.

View Labs

Key Concepts

Delayed Cellular Toxicity (Time-Dependent Effects)

The consequences of inhibiting transcription are not immediately apparent because the cellular machinery continues to function until the reservoir of vital proteins and mRNAs is depleted. This results in a lag phase, during which symptoms may temporarily improve before the critical loss of cellular function, particularly in sensitive organs, leads to organ failure and death.

RNA Polymerase II Inhibition

Eukaryotic RNA polymerase II is the enzyme responsible for synthesizing messenger RNA during transcription. When a toxin binds to this enzyme, it blocks the process of transcription elongation, preventing the production of new mRNAs that are essential for protein synthesis and cell function.

Protein Turnover and Cellular Reserve

Even though transcription is inhibited, cells have a reserve of pre-existing proteins and mRNAs that can temporarily sustain their functions. The delay in the manifestation of toxicity is due to the time required for these existing molecules to degrade naturally without being replaced, eventually leading to cellular dysfunction and death.

Transcript

Please give Ace some feedback