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. 2022 Feb 23;18(2):e1010082. doi: 10.1371/journal.pgen.1010082

Correction: Bacterial recognition by PGRP-SA and downstream signalling by Toll/DIF sustain commensal gut bacteria in Drosophila

Shivohum Bahuguna, Magda Atilano, Marcus Glittenberg, Dohun Lee, Srishti Arora, Lihui Wang, Jun Zhou, Siamak Redhai, Michael Boutros, Petros Ligoxygakis
PMCID: PMC8865663  PMID: 35196315

Fig 6 is incorrect. The authors have provided a corrected version here.

Fig 6. Loss of PGRP-SA increases intestinal fat levels.

Fig 6

Loss of PGRP-SA increased intestinal triglyceride levels in 5-day old flies. This phenomenon was suppressed with pharmacological inhibition (rapamycin) or RNAi against TOR in ECs. This was dependent on 4EBP as yw seml; NP1>4E-BPRNAi treated with rapamycin had fat levels statistically indistinguishable from yw seml. N = 15/genotype/treatment a total of three independent experiments (each with n = 5/genotype/treatment). Values of mutants and controls were statistically compared using student’s t-test (***p<0.001, all other comparisons non-significant except yw seml; NP1>4E-BPRNAi treated with rapamycin compared to yw, which has a p value<0.001-comparison not shown in the graph).

Reference

  • 1.Bahuguna S, Atilano M, Glittenberg M, Lee D, Arora S, Wang L, et al. (2022) Bacterial recognition by PGRP-SA and downstream signalling by Toll/DIF sustain commensal gut bacteria in Drosophila. PLoS Genet 18(1): e1009992. doi: 10.1371/journal.pgen.1009992 [DOI] [PMC free article] [PubMed] [Google Scholar]

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