Despite the vast diversity of cellular morphologies found in nature, all eukaryotic cells are composed of a similar set of subcellular structures. A key aspect of cellular diversity is the ability to modify these common structures (e.g., mitochondria, cilia/flagella, and the mitotic spindle) into highly specialized machines that perform specific functions. To understand how different cell types arise, we must understand how cells tune the size and shape, as well as the number of their subcellular parts. The focus of our research is to determine the mechanisms cells use to control and scale the morphological features of their subcellular structures with key aspects of the cell’s geometry.

How does network geometry enable size control?

Cytoskeletal filaments either grow through the addition of their molecular building blocks, or shrink through their removal. To understand how the size, or length, of these filaments are controlled, many studies have sought to identify the nature of the feedback that controls the rates of these competing processes. Our recent work studying how budding yeast controls the length of their actin cables challenges this perspective by presenting a novel, feedback-independent mechanism of length control. This work demonstrates that the geometric arrangement of the filaments that make up higher order cytoskeletal structures is sufficient to encode their own size control. To understand the molecular mechanisms that underlie this control system, we use an integrated approach that includes microscopy, genetics, biochemistry, and computational methods.

How is actin cable length scaled to match cell length?

In addition to controlling the length of their actin cables, budding yeast are also able to scale the size of these cables so that their length matches the length of the cell in which they are assembled. This scaling arises from the manner in which actin cables are assembled – initially actin cables grow fast, but as they elongate their growth progressively slows down. We found that this deceleration behavior of actin cables is cell length dependent, allowing longer cells to assemble longer cables. Currently, we are investigating the molecular mechanisms that allow these cells integrate information about their size (i.e., their length) into the actin cable length control mechanism.