Abstract
The Hippo pathway is an evolutionarily conserved pathway crucial for regulating tissue size and for limiting cancer development. However, recent work has also uncovered key roles for the mammalian Hippo kinases, Mst1/2, in driving appropriate immune responses by directing T cell migration, morphology, survival, differentiation, and activation. In this review, we discuss the classical signaling pathways orchestrated by the Hippo signaling pathway, and describe how Mst1/2 direct T cell function by mechanisms not seeming to involve the classical Hippo pathway. We also discuss why Mst1/2 might have different functions within organ systems and the immune system. Overall, understanding how Mst1/2 transmit signals to discrete biological processes in different cell types might allow for the development of better drug therapies for the treatments of cancers and immune-related diseases.
Highlights
The evolutionarily conserved Hippo pathway was first identified in Drosophila and comprises several kinases, adaptor proteins, and transcription factors
The conjugation between Mst1−/− immature CD4+ SP and cognate Aire+ICAM-1+ mTEC is unstable, due to defective ICAM-1/LFA-1 clustering [26]. These findings collectively provide evidence that Mst1 plays an important role in LFA-1/ICAM-1-related thymocyte migration and antigen recognition, regulating the T cell development in thymus
These differences may be accounted for by a non-canonical function of Mst1/2, as Lats1/2 and YAP functions are not known to be regulated by Mst1 in T cells. These findings indicate that Mst1 signaling pathway is special in lymphocytes and the mechanism it functions in the regulation of lymphocyte proliferation and apoptosis is not clearly illustrated
Summary
The evolutionarily conserved Hippo pathway was first identified in Drosophila and comprises several kinases, adaptor proteins, and transcription factors. As Mst1/2 deficiency leads to impaired Rac1 or RhoA activity, it appears Mst1 plays a role of “relay station” in these signaling pathways to influence cell migration following chemokine stimulation.
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