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La quiralidad molecular al organismo es inducida por la miosina 1D conservada
G Lebreton1, C Géminard1, F Lapraz1
1Université Côte D'Azur, CNRS, Inserm, Institut de Biologie Valrose, Nice, France.
Science (New York, N.Y.)
|November 24, 2018
Resumen
El estudio revela que la Drosophila myosin 1D (Myo1D) rompe la simetría biológica al torcer las células y los cuerpos. Este motor molecular
Área de la Ciencia:
- Biología del desarrollo
- Biología celular
- La biofísica
Sus antecedentes:
- Los sistemas biológicos exhiben asimetría en múltiples escalas, desde moléculas hasta organismos.
- La relación entre estas asimetrías de varios niveles no se entiende bien.
- Comprender la ruptura de simetría es crucial para los procesos de desarrollo.
Objetivo del estudio:
- Investigar los mecanismos moleculares subyacentes a la generación de asimetría de novo en los sistemas biológicos.
- Para identificar los motores moleculares específicos responsables de la torsión direccional.
- Para explorar el papel de las miosinas en la ruptura de la simetría en diferentes niveles biológicos.
Principales métodos:
- Utilizó Drosophila melanogaster como organismo modelo.
- Investigó la función de la miosina 1D (Myo1D) y la miosina 1C (Myo1C) en la torsión celular y del organismo.
- Se realizaron experimentos in vitro para analizar la dinámica de deslizamiento del filamento de actina.
Principales resultados:
- La miosina 1D (Myo1D) y la miosina 1C (Myo1C) pueden inducir torsión direccional en células, órganos y cuerpos enteros.
- La direccionalidad de la torsión está determinada por el dominio motor de la miosina y es intercambiable entre Myo1D y Myo1C.
- Myo1D promueve el deslizamiento en sentido contrario a las agujas del reloj de los filamentos de actina in vitro.
Conclusiones:
- La miosina 1D (Myo1D) actúa como un determinante quiral capaz de romper la simetría en todas las escalas biológicas.
- La interacción quiral entre Myo1D y el citoesqueleto de actina es el mecanismo fundamental para la asimetría de novo.
- Estos hallazgos proporcionan una base molecular para comprender cómo surge la asimetría en los organismos vivos.
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