Protein translation can fluidize bacterial cytoplasm

Area of Science:

• Cellular Biology
• Biophysics
• Molecular Dynamics

Background:

• Bacterial cytoplasm is crowded with macromolecules, leading to size-dependent glassy dynamics.
• Cellular metabolic activities are known to counteract this glassy nature, maintaining essential fluidity.
• The precise mechanisms behind size-dependent glassy dynamics and metabolic fluidization remain unclear.

Purpose of the Study:

• To investigate the origins of size-dependent glassy dynamics in bacterial cytoplasm.
• To elucidate how cellular metabolic activity, specifically protein synthesis, fluidizes the cytoplasm.
• To provide a computational and experimental basis for understanding cytoplasmic fluidity.

Main Methods:

• Utilized computational modeling and targeted experiments.
• Employed Brownian dynamics simulations of an in silico system.
• Analyzed the diffusive states and transitions of ribosomes and polysomes.

Main Results:

• Entropic segregation of protein synthesis machinery causes size-dependent molecular organization and crowding.
• This crowding results in size-dependent glassy dynamics within the cytoplasm.
• Simulations show protein synthesis significantly enhances macromolecular mobility through ribosome state transitions.

Conclusions:

• Protein synthesis machinery segregation drives size-dependent cytoplasmic crowding and glassy dynamics.
• Ribosome dynamics, shifting between free subunits and polysomes, are key to cytoplasmic fluidization.
• Ribosomal protein synthesis is a primary metabolic mechanism for maintaining bacterial cytoplasmic fluidity.