Publication highlights

Lysosomes are cellular organelles containing a potent cocktail of digestive enzymes—proteases—used to break down worn out cell parts and destroy invading viruses and bacteria. There is crosstalk between lysosomes and mitochondria, the energy generating organelles of cells, but whether this cross talk is affected by lysosomal damage is unknown. In a collaboration led by the Gutierrez lab, Bussi et al uncovered a pathway whereby protease leakage from functional lysosomes degrades mitochondrial proteins and impairs human macrophage metabolism, relevant to several diseases where compromise of the lysosomal membranes is a key intracellular event. This work uncovers an inter-organelle communication pathway, providing a general mechanism by which macrophages undergo mitochondrial metabolic reprogramming after membrane damage to the network of intercellular organelles.

In this work we mined this database to refine hESC culture conditions. These data will be a powerful resource for the community and will lead to changes in how hESCs are cultured in the future. Building on these data, we demonstrated that IGF1-receptor/PI3K/AKT, but not FGF receptor, signalling is required for hESC self-renewal. We built a searchable website that includes a compendium of human embryo gene expression analysis and compiled a list of all possible ligand and receptor interactions.