4 research outputs found
The need to account for cell biology in characterizing predatory mixotrophs in aquatic environments
Photosynthesis in eukaryotes first arose through phagocytotic processes wherein an engulfed cyanobacterium was not digested, but instead became a permanent organelle. Other photosynthetic lineages then arose when eukaryotic cells engulfed other already photosynthetic eukaryotic cells. Some of the resulting lineages subsequently lost their ability for phagocytosis, while many others maintained the ability to do both processes. These mixotrophic taxa have more complicated ecological roles, in that they are both primary producers and consumers that can shift more towards producing the organic matter that forms the base of aquatic food chains, or towards respiring and releasing CO2. We still have much to learn about which taxa are predatory mixotrophs as well as about the physiological consequences of this lifestyle, in part, because much of the diversity of unicellular eukaryotes in aquatic ecosystems remains uncultured. Here, we discuss existing methods for studying predatory mixotrophs, their individual biases, and how single-cell approaches can enhance knowledge of these important taxa. The question remains what the gold standard should be for assigning a mixotrophic status to ill-characterized or uncultured taxa—a status that dictates how organisms are incorporated into carbon cycle models and how their ecosystem roles may shift in future lakes and oceans
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Genetic and Transcriptomic Characterization of Arsenic Resistance Mechanisms in Citrobacter sp. TSA-1
This study focuses on Citrobacter sp. TSA-1, an arsenate-reducing bacterium found in termites. Initially expecting an ArrA-type respiratory arsenate reductase, genome sequencing revealed the absence of the arr gene cluster. It was then hypothesized that TSA-1 utilizes an ArsC for both arsenate-mediated growth and reduction.Despite the absence of arsC1, TSA-1 was still capable of arsenate reduction, albeit with reduced resistance. This study aimed to understand arsenic toxicity in TSA-1 and identify alternative arsenate reduction pathways, using molecular microbiology, analytical chemistry, and transcriptomics.
Chapters reviewed arsenic detoxification mechanisms in bacteria, emphasizing their impact on human health. Arsenate and arsenite resistance patterns in Citrobacter sp. TSA-1 ∆arsC1 hinted at an unidentified arsenate reductase. Bioinformatic tools identified two putative arsC genes, arsC2 and arsC3. I show evidence that ArsC3 has no reductase activity. The chapters explored the impact of arsenate and arsenite exposure on TSA-1 transcriptomics and the consequences of losing the main arsenate reductase. Hypotheses anticipated negative effects on cell health, validated by experimental findings.
This study enhances understanding of arsenic detoxification in Citrobacter sp. TSA-1, paving the way for intriguing hypotheses about arsenic exposure effects on bacterial cells under anaerobic conditions
A protease and a lipoprotein jointly modulate the conserved ExoR-ExoS-ChvI signaling pathway critical in Sinorhizobium meliloti for symbiosis with legume hosts.
Sinorhizobium meliloti is a model alpha-proteobacterium for investigating microbe-host interactions, in particular nitrogen-fixing rhizobium-legume symbioses. Successful infection requires complex coordination between compatible host and endosymbiont, including bacterial production of succinoglycan, also known as exopolysaccharide-I (EPS-I). In S. meliloti EPS-I production is controlled by the conserved ExoS-ChvI two-component system. Periplasmic ExoR associates with the ExoS histidine kinase and negatively regulates ChvI-dependent expression of exo genes, necessary for EPS-I synthesis. We show that two extracytoplasmic proteins, LppA (a lipoprotein) and JspA (a lipoprotein and a metalloprotease), jointly influence EPS-I synthesis by modulating the ExoR-ExoS-ChvI pathway and expression of genes in the ChvI regulon. Deletions of jspA and lppA led to lower EPS-I production and competitive disadvantage during host colonization, for both S. meliloti with Medicago sativa and S. medicae with M. truncatula. Overexpression of jspA reduced steady-state levels of ExoR, suggesting that the JspA protease participates in ExoR degradation. This reduction in ExoR levels is dependent on LppA and can be replicated with ExoR, JspA, and LppA expressed exogenously in Caulobacter crescentus and Escherichia coli. Akin to signaling pathways that sense extracytoplasmic stress in other bacteria, JspA and LppA may monitor periplasmic conditions during interaction with the plant host to adjust accordingly expression of genes that contribute to efficient symbiosis. The molecular mechanisms underlying host colonization in our model system may have parallels in related alpha-proteobacteria