Holidays are always focused on food, and this month we turn our attention to the ways that cells process information on, and respond to, nutrient abundance. In all eukaryotes, the presence of nutrients, such as amino acids, is detected by receptors on the surface of the cell, which activate signalling pathways that ultimately lead to cell growth and proliferation, the accumulation of energy or quiescence. Nutrient abundance is coupled to these cell responses by the kinase mammalian target of rapamycin (mTOR). As discussed by Sabatini and colleagues on page 21, recent studies have furthered our understanding of the regulation and function of this signalling pathway and have revealed that its dysregulation can lead to diabetes, cancer and ageing. However, mTOR is not the only kinase that can link nutrient availability and cellular outcome. Three recently published papers, discussed in our Research Highlights section (page 4), report that, in haematopoietic stem cells, the kinase LKB1 can couple information on nutrient availability to cell growth in an mTOR-independent manner.
Nutrient deprivation in a cell activates autophagy - the self-eating of cellular components, such as organelles, to generate energy. Autophagy can also selectively degrade cargo to regulate organelle number or maintain quality control. On page 9, Youle and Narendra focus on mitophagy, the selective degradation of mitochondria. They discuss the molecular mechanisms of mitophagy in yeast and during red blood cell differentiation, and describe how mutations in two proteins regulating mitophagy, PINK1 and parkin, are linked to Parkinson's disease.
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