Munson Michael J, Ganley Ian G
a MRC Protein Phosphorylation and Ubiquitylation Unit; College of Life Sciences; University of Dundee ; Dundee , UK.
Autophagy. 2015;11(12):2375-6. doi: 10.1080/15548627.2015.1106668.
A key point in starvation-induced autophagy occurs at the end of the process, where lysosomes are regenerated from autolysosomes through a pathway termed autophagic lysosome reformation (ALR). ALR occurs when autolysosomal MTOR becomes reactivated by amino acids derived from the autophagic delivery of protein cargo. This activation not only turns off autophagosome formation but also leads to reformation of lysosomes, ready for the next round of autophagy, through a series of events involving autolysosomal tubulation. We have now found that MTOR regulates multiple steps of ALR including direct activation of the PIK3C3-UVRAG lipid kinase complex to enable autolysosomal tubules to break away and regenerate lysosomes.
饥饿诱导自噬的一个关键点发生在该过程的末期，此时溶酶体通过一种称为自噬溶酶体重塑（ALR）的途径从自噬溶酶体中再生。当自噬溶酶体的MTOR被自噬传递的蛋白质货物衍生的氨基酸重新激活时，就会发生ALR。这种激活不仅会关闭自噬体的形成，还会通过一系列涉及自噬溶酶体成管的事件，导致溶酶体重塑，为下一轮自噬做好准备。我们现在发现，MTOR调节ALR的多个步骤，包括直接激活PIK3C3-UVRAG脂质激酶复合物，以使自噬溶酶体小管脱离并再生溶酶体。
