FOCAL POINT A team of researchers led by Ira Mellman, Bryan Lo, and Geraldine Strasser (pictured, left to right, with statues of Genentech founders Bob Swanson and Herb Boyer) examine how the kinase Lkb1 contributes to tissue morphogenesis and the early stages of cancer development. The researchers generated mice expressing a mutant version of Lkb1 that can be reversibly inhibited by the ATP analog 1NMPP1. By culturing organs from these mice, Lo et al. reveal that Lkb1 regulates branching morphogenesis in the lung via an AMPK-dependent pathway, whereas, in the pancreas, Lkb1 inhibition induces the formation of epithelial cysts and precancerous lesions independently of AMPK. In both tissues, loss of Lkb1 activity fails to disrupt cell polarity. Pancreatic lesions induced by Lkb1 inhibition (right) show the same pattern of apical actin (red) and basolateral EpCAM (green) as the acini from a control pancreas (center). / PHOTO COURTESY OF CECILE CHALOUNI

FOCAL POINT A team of researchers led by Ira Mellman, Bryan Lo, and Geraldine Strasser (pictured, left to right, with statues of Genentech founders Bob Swanson and Herb Boyer) examine how the kinase Lkb1 contributes to tissue morphogenesis and the early stages of cancer development. The researchers generated mice expressing a mutant version of Lkb1 that can be reversibly inhibited by the ATP analog 1NMPP1. By culturing organs from these mice, Lo et al. reveal that Lkb1 regulates branching morphogenesis in the lung via an AMPK-dependent pathway, whereas, in the pancreas, Lkb1 inhibition induces the formation of epithelial cysts and precancerous lesions independently of AMPK. In both tissues, loss of Lkb1 activity fails to disrupt cell polarity. Pancreatic lesions induced by Lkb1 inhibition (right) show the same pattern of apical actin (red) and basolateral EpCAM (green) as the acini from a control pancreas (center).

PHOTO COURTESY OF CECILE CHALOUNI

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