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Other examples of efflux pumps involved in bacteria/plant interactions are highlighted below. In A. tumefaciens, the IfeAB efflux pump is involved in the competitive colonization of alfalfa roots and can confer measurable ecological benefits to these bacteria in an environment where flavonoids are present [114]. The EmrAB efflux system in S. meliloti is induced by flavonoids and bacterial symbiosis with Medicago sativa is impaired when emrR, the gene encoding the TetR repressor of this efflux pump, is deleted [115,119]. Another multidrug efflux system of S. meliloti that plays an important role in nodulation competitiveness by mediating resistance toward antimicrobial compounds produced by the host plant is SmeAB [120]. The BjG30 efflux pump from B. japonicum may play a role in the early stage of symbiosis of this microorganism with soybean by balancing the dual functions of genistein as both a nod gene inducer and as a toxic compound [112]. Notably, B. japonicum presents another efflux pump, BdeAB, which seems to be involved in the symbiotic nitrogen-fixation activity of this microorganism in soybean; mutants deficient in this efflux pump, in addition of presenting symbiotic defects, are more susceptible to aminoglycosides [121], showing that antibiotic resistance is interlinked with other relevant functions of efflux pumps. Erwinia chrysanthemi is another example of the need of efflux pumps to colonize plant tissues. The infection by E. chrysanthemi causes salicylic acid accumulation in the host, leading to an amplification of the plant defence response and the production of pathogenesis-related proteins and toxic antimicrobial compounds. The combination of salicylic acid and its precursors activates the expression of multidrug efflux pump-encoding genes and enhances the survival of the bacterium [122].
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It is important to highlight that efflux pumps may play a double functional role by modulating bacteria/plant and intermicrobial interactions. Indeed, a tolC mutant of E. chrysanthemi is defective in the efflux of berberine, an antimicrobial plant compound, and it is unable to cause plant tissue maceration in planta. In addition, this mutant is impaired for competing with the microbial community present in the same ecosystems, indicating that these efflux pumps have a role in microbial interspecific competition [123]. In line with the potential role of efflux pumps on bacterial competition, it has been shown that an E. chrysanthemi mutant defective in the ABC transporter YbiT conserves virulence in potato tubers but is less infectious than the wild type strain when growing together with saprophytic bacteria such as P. fluorescens or P. putida, possibly because this efflux pump can extrude toxic compounds produced by these bacteria [124].
Another important gut pathogen is Campylobacter jejuni. Among the known antibiotic resistance mechanisms of this microorganism, the CmeABC efflux pump is a relevant player and confers resistance to structurally-diverse antibiotics and toxic compounds [138], including those naturally present in its animal host, as bile salts [130]. CmeABC belongs to the RND family of efflux transporters and its expression is regulated by the transcriptional repressor CmeR, which binds to a specific site in the promoter region of cmeABC [139]. As it happens in the case of acrAB, bile salts, which are natural substrates of this efflux pump, are able to induce expression of cmeABC, promoting the dissociation of CmeR from its operator and allowing the transcription of the operon [139]. Induction by cholate, an unconjugated bile salt, is fully CmeR-dependent; however, induction by taurocholate, a conjugated bile salt, is not attributable to the release of CmeR-mediated repression, suggesting a CmeR-independent pathway. Induction of this efflux pump by bile salts confers resistance to diverse antibiotics, including cefotaxime, novobiocin, ciprofloxacin, and erythromycin. As in the case of Salmonella (see above), the presence of bile salts in the gut may decrease the susceptibility of C. jejuni to antibiotics in vivo. Like in the case of acrAB, salicylate also induces the expression of cmeABC in C. jejuni and promotes the emergence of quinolone-resistant mutants in this bacterial species [140]. This induction can be explained by the fact that salicylate inhibits the binding of CmeR to its operator DNA, although this inhibition is weaker than in the presence of bile salts.
The fact that the expression of MDR efflux pumps is induced by host-produced compounds suggests that they can play a role in the virulence of bacterial pathogens, a possibility that was discussed a decade ago [148]. Indeed, it has been shown that the Vibrio cholerae efflux pump VexB is the primary efflux system responsible for resistance to bile salts in this microorganism [149]. Since bile salts are present at the human gut, the activity of this efflux pump is a pre-requisite for V. cholerae infection. A similar situation happens with AcrAB, the main pump responsible for bile salts resistance in Enterobacteriaceae [150], which is required for the pathogenesis of Salmonella enterica serovar Typhimurium [151]. Notably this efflux pump is involved as well in the bacterial capability for forming biofilms [152,153]. A protective role to host antibacterial compounds has also been described in the case of Neisseria gonorrhoeae. In this organism, the MtrCDE efflux pump contributes to resistance to vertebrate antibacterial peptides [132,154], and FarAB is involved in resistance to long-chain fatty acids [155]. The activity of these efflux pumps contributes to the pathogenesis of N. gonorrhoeae [154,156]. Similarly, the Campylobacter jejuni CmeABC efflux pump confers resistance to bile salts, fatty acids, and detergents, and is needed for the colonization of the intestinal tract [157].
Federal Reserve lending to depository institutions (the "discount window") plays an important role in supporting the liquidity and stability of the banking system and the effective implementation of monetary policy. By providing ready access to funding, the discount window helps depository institutions manage their liquidity risks efficiently and avoid actions that have negative consequences for their customers, such as withdrawing credit during times of market stress. Thus, the discount window supports the smooth flow of credit to households and businesses. Providing liquidity in this way is one of the original purposes of the Federal Reserve System and other central banks around the world.
The rule is based on a notice of proposed rulemaking issued on May 21, 1997. See 62 FR 27900. The rule is issued pursuant to Congressional direction in both the Money Laundering Suppression Act of 1994 and Annunzio-Wylie Anti-Money Laundering Act of 1992. It completes the second rulemaking relating to the application of the BSA to MSBs under the 1992 and 1994 laws begun on May 21, 1997. The first rulemaking resulted in a final rule, published on August 18, 1999, that revises the definition of certain businesses for BSA purposes and requires MSBs to register with the Department of the Treasury. See 64 FR 45438. It should be noted that, under the BSA, MSBs are currently required to report to FinCEN cash transactions exceeding $10,000. The information plays a key role in helping law enforcement investigators follow the money trail of criminals.
As we look toward the end of 2022, we suggest investors gradually take on more interest rate risk while remaining cautious about credit risk. If the economy and Fed policy play out as we expect, then 10-year Treasury yields are likely to trend lower over the long run. However, lower credit quality bonds may weaken because they are exposed to a potential downturn in the economy.
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