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La abscisión citokinética mediada por P2 previene la senescencia temprana y la formación de cataratas

Federico Gulluni¹, Lorenzo Prever¹, Huayi Li¹

¹Department of Molecular Biotechnology and Health Sciences, University of Turin, Turin 10126, Italy.

Science (New York, N.Y.)

|December 9, 2021

Resumen

Una vía conservada que involucra a PI3K-C2α, PI(3,4) P2 y ESCRT-II (VPS36) regula la división celular del cristalino. La interrupción de este proceso afecta la citocinesis, lo que lleva a la senescencia prematura y la aparición temprana de cataratas en los vertebrados.

Área de la Ciencia:

Biología celular
Biología molecular
Oftalmología

Sus antecedentes:

La abscisión de la membrana citokinética es crucial para la división celular, regulada por la maquinaria ESCRT en el cuerpo medio.
La disfunción del ESCRT está relacionada con la catarata, pero los mecanismos específicos siguen sin estar claros.

Objetivo del estudio:

Elucidar el mecanismo que vincula la función de los TECS, la citocinesis y la formación de cataratas en el cristalino.
Identificar los actores moleculares clave en la citocinesis específica de las lentes.

Principales métodos:

Investigó un proceso citokinético específico de lentes en peces, ratones y modelos humanos.
Se utilizaron enfoques genéticos y moleculares para evaluar las funciones de PI3K-C2α, PI(3,4) P2 y VPS36.

Principales resultados:

Se identificó una vía que requiere PI3K-C2α, su producto PI(3,4) P2 y la subunidad ESCRT-II VPS36 para la citocinesis de las células del cristalino.
La pérdida de estos componentes dio lugar a un deterioro de la citocinesis y a una senescencia prematura de las células del cristalino.
Se ha demostrado la conservación evolutiva de esta vía en todas las especies.

Conclusiones:

Una vía conservada y específica para el lente que involucra a PI3K-C2α, PI(3,4) P2 y VPS36 es esencial para prevenir la senescencia prematura y la aparición temprana de cataratas.
Esta vía destaca un nuevo mecanismo para el control de la citoquinesis específica del tipo de célula.

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