Taylor Hinnant

Research

The cell biology of small intestine development and homeostasis...

The small intestine is a looping tube within the gastrointestinal tract. The outer portion of the tube consist of smooth muscle. The inner portion of the tube consists of epithelial cells and supporting mesenchyme. The adult intestinal epithelia is divided into two compartments, the villi, which form protrusions into the lumen of the intestine and contain postmitotic, undifferentiated cells that largely function in nutrient absorption. And the crypt, which protrudes into the mesenchyme and contains proliferating cells that will give rise to the specialized cells of the villi. The cells in the crypt are proliferating constantly, causing very fast turnover of villar cells. I use the mouse intestine to study how specific cytoskeletal structures affect the ability for this organ to develop and maintain its proper shape and size.

Actin-myosin contractility in differentiated cells regulates intestine morphology and stem cell activity

Previous studies have shown that infection with pathogens such as Salmonella activate prompt myosin-mediated contractions of intestine epithelial cells. We directly tested the physiological consequences of villar cell contractility in vivo by genetically inducing myosin activation through overexpression of an Arhgef11 transgene. Contraction of differentiated cells elicits a systemic increase in proliferation of cells in the crypt compartment, leading to longer crypts. Interestingly crypt depth increase has been associated with Salmonella infection in mutant intestinal tissue. However cell contraction does not lead to increased immune cell infiltration or epithelial barrier defects that have been previously associated with pathogen infection-induced crypt proliferation increase.

Actin-myosin contractility in mesenchyme cells of the fetal intestine regulate villi development

The contractile state of mesenchyme cells has been shown to regulate their activity as well as their ability to support associated cell types. We genetically induced actin-myosin contractility specifically in the mesenchyme during the development of villi structures and found that it leads to an increased number of mesenchyme cells. Overall, this leads to wider villi structures that fail to form properly elongated villi by the time of birth.

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