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Las estructuras cryo-EM capturan el ciclo de transporte de la flipase P4-ATPase

Masahiro Hiraizumi^1,2, Keitaro Yamashita^1,3, Tomohiro Nishizawa⁴

¹Department of Biological Sciences, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.

Science (New York, N.Y.)

|August 17, 2019

Resumen

Los investigadores aclararon el ciclo de translocación lipídica de las P4-ATPasas humanas utilizando microscopía criolectrónica. Esto revela cómo estas proteínas vitales de la membrana transportan fosfolípidos y mantienen la asimetría celular.

Área de la Ciencia:

Biología de las membranas
Biología estructural
La bioquímica

Sus antecedentes:

Las ATPasas tipo P tipo IV (P4-ATPasas) son cruciales para mantener la asimetría lipídica de la membrana eucariota.
La asimetría lipídica es esencial para el tráfico de membranas y las vías de señalización celular.

Objetivo del estudio:

Determinar las estructuras de distintos productos intermedios en el heterocomplejo humano ATP8A1-CDC50a P4-ATPasa.
Para aclarar el mecanismo de la translocación de fosfolípidos mediada por las P4-ATPases.

Principales métodos:

Se utilizó la criomicroscopia electrónica (Cryo-EM) para obtener estructuras.
Se determinaron estructuras de alta resolución (2,63,3 angstroms) de seis productos intermedios distintos.

Principales resultados:

El estudio revela cambios conformacionales dependientes del ATP, incluido el movimiento rotacional del dominio del actuador y los desplazamientos laterales de las hélices transmembranales.
Estos cambios estructurales facilitan la unión y translocación de la fosfatidilserina a través de la membrana.
El grupo principal de fosfolípidos se mueve a través de una hendidura hidrófila, mientras que la cadena acil interacciona con el entorno lipídico.

Conclusiones:

Los hallazgos proporcionan información a nivel atómico sobre el mecanismo de la flipasa de la P4-ATPasa.
Comprender este mecanismo es vital para comprender el transporte de lípidos y las enfermedades asociadas causadas por mutaciones de la P4-ATPasa.

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