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Fig. 10. A model for the role of PTEN in the suppression of lateral pseudopod formation. In the absence and in the presence of attractant, PTEN localizes constitutively at the same level in the cortex of the main cell body. (A) In the absence of attractant, a low steady state level of MHC-dephosphorylation results in myosin II and F-actin localization in the cortex with PTEN. This steady state localization is responsible for the suppression of lateral pseudopod formation through the generation of cortical tension. Once every 2 minutes in the absence of attractant, a lateral pseudopod forms randomly, usually from the anterior half of the cell body at a site where the myosin II-F-actin cortex transiently weakens. (B) In response to the increasing temporal and positive spatial gradients of attractant in the front of wave, a receptor-mediated signal transduction pathway is activated that increases the rate of myosin II dephosphorylation, resulting in an increase in cortical myosin II and F-actin. This results in an increase in cortical tension, leading to the increased suppression of lateral pseudopod formation in the front of a wave. In this model, receptor-mediated dephosphorylation of MHC is responsible for increased cortical tension. The similar behavioral defects of the mutants myoA, myoB, myoF, clathrin and sphingosine-1-phosphate lyase suggest that they also play roles in steady state pseudopod suppression in the absence of attractant and increased suppression in the front of a wave. In the model, PTEN is essential for myosin II-F-actin localization and pseudopod suppression in the absence of attractant, and the increases in localization and suppression in the front of the wave. But because it remains at a constitutive level in the cortex, it has not been placed in the receptor-activated transduction pathway leading to increased pseudopod suppression. It should be emphasized that this model deals with a mechanism that affects the efficiency of the chemotactic response through lateral pseudopod suppression, not with a mechanism of gradient sensing or the maintenance of cellular polarity.
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