GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314574/primaryOK200TranscriptomicsAcinetobacter baumanniiExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314574GEOGSEfalseOuter membrane remodeling via lipid-peptidoglycan crosstalk enables lipooligosaccharide-deficient colistin resistanceAlthough several Acinetobacter baumannii lineages can acquire colistin resistance by eliminating LPS/LOS glycolipids, the widely used reference background ATCC 17978 is unable to access this trajectory under standard selection, suggesting that glycolipid essentiality is strongly context dependent. Here we show that this barrier is not absolute but instead reflects the structural state of the envelope. Disrupting phospholipid homeostasis, through loss of the Mla system, which mediates retrograde phospholipid transport, and the outer-membrane phospholipase PldA, which degrades mislocalized phospholipids, destabilizes lipid asymmetry and creates a fragile yet permissive state that enables the emergence of stable glycolipid-deficient, colistin-resistant variants.2026/06/03GSE314574GSM9402166GSM9402165GSM9402175GSM9402164GSM9402174GSM9402169GSM9402168GSM9402167GSM9402173GSM9402172GSM9402171GSM940217034857314574Acinetobacter baumannii