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The purple non-sulfur bacterium Rhodopseudomonas palustris TIE-1 can produce useful biochemicals such as bioplastics and biobutanol. Production of such biochemicals requires intracellular electron availability, which is governed by the availability and the transport of essential metals such as iron (Fe). Because of the distinct chemical properties of ferrous [Fe(II)] and ferric iron [Fe(III)], different transport systems are required for their transport and storage in bacteria. Although Fe(III) transport systems are well characterized, we know much less about Fe(II) transport systems except for the FeoAB system. Iron transporters can also import manganese (Mn). Here, we study Fe and Mn transport by five putative Fe transporters in TIE-1 under metal-replete, -deplete, oxic and anoxic conditions. We observe that by overexpressing feoAB, efeU, and nramp1AB, the intracellular concentration of Fe and Mn can be enhanced in TIE-1, under oxic and anoxic conditions, respectively. The deletion of a single gene/operon dintracellular electron availability, which in turn is mediated by various iron-containing proteins in the cell. Several putative Fe transporters exist in TIE-1’s genome. Some of these transporters can also transport Mn, part of several important cellular enzymes. Therefore, understanding the ability to transport and respond to varying levels of Fe and Mn under different conditions is important to improve TIE-1’s ability to produce useful biomolecules. Our data suggest that by overexpressing Fe transporter genes via plasmid-based expression, we can increase the import of Fe and Mn in TIE-1. Future work will leverage these data to improve TIE-1 as an attractive microbial chassis and future biotechnological workhorse.Bacterial alkane metabolism is associated with a number of cellular stresses, including membrane stress, oxidative stress, and the limited uptake of charged ions such as sulfate. In the present study, the genes ssuD and tauD in Acinetobacter oleivorans DR1 cells, which encode an alkanesulfonate monooxygenase and a taurine dioxygenase, respectively, were found to be responsible for hexadecanesulfonate (C16SO3H) and taurine metabolism, and Cbl was experimentally identified as a potential regulator of ssuD and tauD expression. The expression of ssuD and tauD occurred under sulfate-limited conditions generated during n-hexadecane degradation. Interestingly, expression analysis and knockout experiments suggested that both genes are required to protect cells against oxidative stress, including that generated by n-hexadecane degradation and H2O2 exposure. Measurable levels of intracellular hexadecanesulfonate were also produced during n- hexadecane degradation. Phylogenetic analysis suggested that ssuD and tauD are mainly present in soil-dwelling aerobes within the β- and γ- proteobacteria classes, which suggests that they function as controllers of the sulfur cycle and play a protective role against oxidative stress in sulfur-limited conditionsIMPORTANCE Alkanesulfonate monooxygenase (ssuD) and taurine dioxygenase (tauD), which play a role in the degradation of organosulfonate, were expressed during n-hexadecane metabolism and oxidative stress conditions in Acinetobacter oleivorans DR1. Our study confirmed that hexadecanesulfonate was accidentally generated during bacterial n-hexadecane degradation in sulfate-limited conditions. Removal of this byproduct by SsuD and TauD must be necessary for bacterial survival under oxidative stress generated during n-hexadecane degradation.Plants mount defense responses by recognizing indicators of pathogen invasion, including microbe-associated molecular patterns (MAMPs). Flagellin, from the bacterial pathogen Pseudomonas syringae pv. tomato (Pst), contains two MAMPs, flg22 and flgII-28, that are recognized by tomato (Solanum lycopersicum) receptors Flagellin sensing 2 (Fls2) and Flagellin sensing 3 (Fls3, respectively, but to what degree each receptor contributes to immunity and if they promote immune responses using the same molecular mechanisms are unknown. Here, we characterized CRISPR/Cas9-generated Fls2 and Fls3 tomato mutants and found the two receptors contribute equally to disease resistance both on the leaf surface and in the apoplast. However, we observed striking differences in certain host responses mediated by the two receptors. Compared to Fls2, Fls3 mediated a more sustained production of reactive oxygen species (ROS) and an increase in transcript abundance of 44 tomato genes, with two genes serving as specific reporters for the Fls3 pathway. Fls3 had greater in vitro kinase activity than Fls2 and could transphosphorylate a substrate. Using chimeric Fls2/Fls3 proteins, we found no evidence that a single receptor domain is responsible for the Fls3 sustained ROS, suggesting involvement of multiple structural features or a nullified function of the chimeric construct. This work reveals differences in certain immunity outputs between Fls2 and Fls3, suggesting they might use distinct molecular mechanisms to activate pattern-triggered immunity in response to flagellin-derived MAMPs.Vivipary, wherein seeds germinate prior to dispersal while still associated with the maternal plant, is an adaptation to extreme environments. Selleck MK-0752 It is normally inhibited by the establishment of dormancy. The genetic framework of vivipary has been well studied; however, the role of epigenetics in vivipary remains unknown. Here, we report that silencing of METHYLTRANSFERASE1 (SlMET1) promoted precocious seed germination and seedling growth within the tomato (Solanum lycopersicum) epimutant Colourless non-ripening (Cnr) fruits. This was associated with decreases in abscisic acid (ABA) concentration and levels of mRNA encoding 9-cis-epoxycarotenoid-dioxygenase (SlNCED), which is involved in ABA biosynthesis. Differentially methylated regions were identified in promoters of differentially expressed genes, including SlNCED. SlNCED knockdown also induced viviparous seedling growth in Cnr fruits. Strikingly, Cnr ripening reversion suppressed vivipary. Moreover, neither SlMET1/SlNCED-VIGS nor transgenic SlMET1-RNAi produced vivipary in wild-type tomatoes; the latter affected leaf architecture, arrested flowering and repressed seed development.