Density-Dependent Inhibition and Anchorage Dependence In Cell Division


Density-dependent inhibition and anchorage dependence of cell division. Individual cells are shown disproportionately large in the drawings. Source: Urry, Lisa A.. Campbell Biology (p. 248). Pearson Education. Kindle Edition.

The effect of an external physical factor on cell division is clearly seen in density-dependent inhibition, a phenomenon in which crowded cells stop dividing. As first observed many years ago, cultured cells normally divide until they form a single layer of cells on the inner surface of a culture flask, at which point the cells stop dividing. If some cells are removed, those bordering the open space begin dividing again and continue until the vacancy is filled. Follow-up studies revealed that the binding of a cell-surface protein to its counterpart on an adjoining cell sends a signal to both cells that inhibits cell division, preventing them from moving forward in the cell cycle, even in the presence of growth factors.

Most animal cells also exhibit anchorage dependence. To divide, they must be attached to a substratum, such as the inside of a culture flask or the extracellular matrix of a tissue. Experiments suggest that like cell density, anchorage is signaled to the cell cycle control system via pathways involving plasma membrane proteins and elements of the cytoskeleton linked to them.

Density-dependent inhibition and anchorage dependence appear to function not only in cell culture but also in the body’s tissues, checking the growth of cells at some optimal density and location during embryonic development and throughout an organism’s life. Cancer cells exhibit neither density-dependent inhibition nor anchorage dependence.

Source:

Urry, Lisa A.. Campbell Biology (p. 247). Pearson Education. Kindle Edition.


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