RESUMEN
Ferroptosis is a form of cell death caused by lipid peroxidation that is emerging as a target for cancer therapy, highlighting the need to identify factors that govern ferroptosis susceptibility. Lipid peroxidation occurs primarily on phospholipids containing polyunsaturated fatty acids (PUFAs). Here, we show that even though extracellular lipid limitation reduces cellular PUFA levels, lipid-starved cancer cells are paradoxically more sensitive to ferroptosis. Using mass spectrometry-based lipidomics with stable isotope fatty acid labeling, we show that lipid limitation induces a fatty acid trafficking pathway in which PUFAs are liberated from triglycerides to synthesize highly unsaturated PUFAs such as arachidonic acid and adrenic acid. These PUFAs then accumulate in phospholipids, particularly ether phospholipids, to promote ferroptosis sensitivity. Therefore, PUFA levels within cancer cells do not necessarily correlate with ferroptosis susceptibility. Rather, how cancer cells respond to extracellular lipid levels by trafficking PUFAs into proper phospholipid pools dictates their sensitivity to ferroptosis.
RESUMEN
Halomonas sp. SSL-5 is a Mn(II)-oxidizing, perchlorate-tolerant halophilic bacterium isolated from an Australian hypersaline lake. The genome sequence contains 27 contigs, and the genome is 3.4 Mb with a GC content of 67.2%. The sequence provides information for future studies of Mn(II) oxidation and perchlorate resistance under halophilic conditions.
RESUMEN
Halomonas sp. strain KAO is an aerobic, Mn(II)-oxidizing, halophilic bacterium. The draft genome of the isolate contains 47 contigs encompassing 3.7 Mb and a GC content of 64.22%. This sequence will provide essential information for future studies of Mn(II) oxidation, particularly under halophilic conditions.
