Paenibacillus plantiphilus sp. nov. from the plant environment of Zea mays.

A Gram-strain positive, aerobic, endospore-forming bacterial strain (JJ-246T) was isolated from the rhizosphere of Zea mays. The 16S rRNA gene sequence similarity comparisons showed a most closely relationship to Paenibacillus oenotherae DT7-4T (98.4%) and Paenibacillus xanthinolyticus 11N27T (98.0%). The pairwise average nucleotide identity and digital DNA-DNA hybridisation values of the JJ-246T genome assembly against publicly available Paenibacillus type strain genomes were below 82% and 33%, respectively. The draft genome of JJ-246T shared many putative plant-beneficial functions contributing (PBFC) genes, related to plant root colonisation, oxidative stress protection, degradation of aromatic compounds, plant growth-promoting traits, disease resistance, drug and heavy metal resistance, and nutrient acquisition. The quinone system of strain JJ-246T, the polar lipid profile and the major fatty acids were congruent with those reported for members of the genus Paenibacillus. JJ-246T was shown to represent a novel species of the genus Paenibacillus, for which the name Paenibacillus plantiphilus sp. nov. is proposed, with JJ-246T (= LMG 32093T = CCM 9089T = CIP 111893T) as the type strain.

Paenibacillus auburnensis sp. nov. and Paenibacillus pseudetheri sp. nov., isolated from the rhizosphere of Zea mays.

Two Gram-stain-positive, aerobic, endospore-forming bacterial strains, isolated from the rhizosphere of Zea mays were studied for their detailed taxonomic allocation. Based on 16S rRNA gene sequence similarity comparisons, both strains JJ-7T and JJ-60T were shown to be members of the genus Paenibacillus. Strain JJ-7T was most closely related to the type strains of Paenibacillus tianjinensis (99.6 %) and P. typhae (98.7 %), and strain JJ-60T to Paenibacillus etheri (99.5 %). The 16S rRNA gene sequence similarities to all other Paenibacillus species were ≤98.4 %. Both strains JJ-7T and JJ-60T showed 97.6 % 16S rRNA gene sequence similarity between each other. Genomic comparisons showed that the average nucleotide identity and digital DNA-DNA hybridization values to next related type strain genomes were always <94 and <56 %, respectively. The polar lipid profiles of both strains contain a number of phospholipids including diphosphatidylglycerol, phosphatidylglycerol and phosphatidylethanolamine, which is in accord with the genus Paenibacillus. The major quinone was MK-7 in both strains. Major fatty acids were iso- and anteiso-branched. Physiological and biochemical characteristics allowed a further phenotypic differentiation of strains JJ-7T and JJ-60T from the most closely related species. Thus, each strain represents a novel species of the genus Paenibacillus, for which the names Paenibacillus auburnensis sp. nov. and Paenibacillus pseudetheri sp. nov. are proposed, with JJ-7T (=CIP 111892T=DSM 111785T=LMG 32088T=CCM 9087T) and JJ-60T (=CIP 111894T=DSM 111787T=LMG 32090T=CCM 9086T) as the type strains, respectively.

Paenibacillus allorhizoplanae sp. nov. from the rhizoplane of a Zea mays root.

A Gram-positive staining, aerobic, endospore-forming bacterial strain, isolated from the rhizosphere of Zea mays was studied for its detailed taxonomic allocation. Based on the 16S rRNA gene sequence similarity comparisons, strain JJ-42 T was shown to be a member of the genus Paenibacillus, most closely related to the type strain of Paenibacillus pectinilyticus (98.8%). The 16S rRNA gene sequence similarity to all other Paenibacillus species was below 98.5%. The pairwise average nucleotide identity (ANI) and digital DNA-DNA hybridization (dDDH) values of the JJ-42 T genome assembly against publicly available Paenibacillus type strain genomes were below 92% and 47%, respectively. The quinone system of strain JJ-42 T consisted exclusively of menaquinone MK-7. The polar lipid profile consisted of the major components diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, three aminophospholipids (APL), and one unidentified lipid. The major fatty acids were iso- and anteiso-branched with the major compound anteiso C15:0. Physiological and biochemical characteristics allowed a further phenotypic differentiation of strain JJ-42 T from the most closely related species. Thus, JJ-42 T represents a novel species of the genus Paenibacillus, for which the name Paenibacillus allorhizoplanae sp. nov. is proposed, with JJ-42 T (= LMG 32089 T = CCM 9085 T = DSM 111786 T = CIP 111891 T) as the type strain.

Altered splicing of ATG16-L1 mediates acquired resistance to tyrosine kinase inhibitors of EGFR by blocking autophagy in non-small cell lung cancer.

Despite the initial efficacy of using tyrosine kinase inhibitors of epidermal growth factor receptors (EGFR-TKIs) for treating patients with non-small cell lung cancer (NSCLC), resistance inevitably develops. Recent studies highlight a link between alternative splicing and cancer drug response. Therefore, we aimed to identify deregulated splicing events that play a role in resistance to EGFR-TKI. By using RNA sequencing, reverse-transcription PCR (RT-PCR), and RNA interference, we showed that overexpression of a splice variant of the autophagic gene ATG16-L1 that retains exon 8 and encodes the ß-isoform of autophagy-related protein 16-1 (ATG16-L1 ß) concurs acquired resistance to EGFR-TKI in NSCLC cells. Using matched biopsies, we found increased levels of ATG16-L1 ß at the time of progression in 3 of 11 NSCLC patients treated with EGFR-TKI. Mechanistically, gefitinib-induced autophagy was impaired in resistant cells that accumulated ATG16-L1 ß. Neutralization of ATG16-L1 ß restored autophagy in response to gefitinib, induced apoptosis, and inhibited the growth of in ovo tumor xenografts. Conversely, overexpression of ATG16-L1 ß in parental sensitive cells prevented gefitinib-induced autophagy and increased cell survival. These results support a role of defective autophagy in acquired resistance to EGFR-TKIs and identify splicing regulation of ATG16-L1 as a therapeutic vulnerability that could be explored for improving EGFR-targeted cancer therapy.