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Señalización antiviral de una desaminasa asociada con CRISPR de tipo III

Yutao Li^1,2, Zhaoxing Li^1,2,3, Purui Yan^1,2

¹Department of Pharmacology, School of Pharmacy, China Pharmaceutical University, Nanjing, China.

Science (New York, N.Y.)

|December 12, 2024

Resumen

Los procariotas usan un sistema CRISPR-Cas para agotar la energía celular (ATP) como una defensa antiviral. Este mecanismo convierte el ATP en ITP, deteniendo el crecimiento celular para combatir las infecciones virales.

Área de la Ciencia:

Microbiología
Biología molecular
La bioquímica

Sus antecedentes:

Los procariotas poseen sofisticados mecanismos de defensa contra los patógenos virales.
Los sistemas CRISPR-Cas y el agotamiento de la reserva de nucleótidos son estrategias antivirales conocidas.

Objetivo del estudio:

Para aclarar un nuevo mecanismo antiviral que involucra el agotamiento del trifosfato de adenosina (ATP) regulado por CRISPR-Cas tipo III.
Caracterizar la base estructural y bioquímica de esta vía de agotamiento del ATP.

Principales métodos:

Se utilizó la crio-microscopia electrónica (cryo-EM) para determinar las estructuras de la adenosina desaminasa asociada a CRISPR-Cas (CAAD).
Se realizaron ensayos bioquímicos para analizar la actividad enzimática del CAAD y su regulación.

Principales resultados:

Se identificó una nueva vía en la que el CAAD activado convierte el ATP en trifosfato de inosina (ITP).
La activación de CAAD por ligandos cíclicos de adenosina (cA4 o cA6) induce cambios conformacionales, liberando autoinhibición y activando la actividad de la desaminasa.
El ITP es posteriormente hidrolizado a monofosfato de inosina (IMP) por Nudix hidrolasa, lo que lleva a la detención del crecimiento celular.

Conclusiones:

Este estudio revela una estrategia antiviral mediada por CRISPR-Cas previamente desconocida basada en el agotamiento de la energía.
Los hallazgos proporcionan información estructural y mecanicista sobre la función de CAAD y su papel en la inmunidad procariótica.

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