U.S. Treasury Secretary Scott Bessent said he isn’t calling for a series of interest-rate cuts from the Federal Reserve, just pointing out that models suggest a “neutral” rate would be about 1.5 percentage points lower.
“I didn’t tell the Fed what to do,” Bessent said Thursday in an interview on Fox Business, referring to his comments a day before about how the central bank “could go into a series of rate cuts here.”
Bessent said Thursday that “what I said was that to get to a neutral rate on interest, that that would be approximately a 150-basis-point cut.”
The so-called neutral rate is the level at which policy neither stimulates nor restricts the economy. Fed Chair Jerome Powell said July 30 that there are “a range of views of what the neutral rate is at this moment for our economy” and that his own estimate was that the current setting was “modestly restrictive.”
“I believe that there is room, if one believes in the neutral rate,” for a series of rate cuts, Bessent said. “I’m not calling for one. I didn’t call for one. I just said that a model of a neutral rate is approximately 150 basis points lower.”
The Fed last month kept its target range for the benchmark rate at 4.25% to 4.5%. The median estimate of the neutral rate among Fed officials over the long run is 3%. Powell and many of his colleagues have for months argued that more time was needed to assess any impact on inflation and inflation expectations from President Trump’s tariff hikes.
Trump has regularly criticized Powell for holding rates. Bessent, after taking the Treasury’s helm, said he would only address past Fed actions, not future ones, but later weighed in on what he thought markets were expecting monetary policymakers to do. This week, he has taken to referring to economic models, and has repeatedly suggested a 50-basis-point rate cut is possible at the Fed’s September meeting.
“It’s not really the role of the Treasury secretary to opine” on the neutral rate, said Julia Coronado, founder of the research firm MacroPolicy Perspectives and a former Fed economist. “The fact that the most senior economic official in the administration is saying these things publicly is direct, public pressure on what he wants the Fed to do.”
Former Treasury Secretary Lawrence Summers, who served under Democratic President Clinton, said he was “surprised” to see Bessent’s remarks on Wednesday.
“Usually that kind of judgment is not made by administration officials, and I’m not sure it’s helpful for the administration to be publicly prescribing on monetary policy,” Summers said on Bloomberg Television’s Wall Street Week with David Westin.
Summers, a paid contributor to Bloomberg TV, also suggested that a measure of the neutral rate should incorporate the effects of large budget deficits and elevated demand for funds to pay for data centers — along with higher asset prices that reduce the flow of funds into savings. Against that backdrop, “you wouldn’t be prescribing a 175-basis-point cut in rates unless we see a recession.”
Interest-rate futures as of Thursday morning reflect bets that the Fed will cut rates by less than a cumulative 150 basis points by the end of next year. They also show slightly less confidence in a 25-basis-point reduction at the September meeting. The retreat came after a release on U.S. wholesale inflation showed those prices climbed by the most in three years.
Speaking to Bloomberg Television on Wednesday, Bessent said “if you look at any model” it suggests that “we should probably be 150, 175 basis points lower” on the Fed’s benchmark. He also said that officials might have cut rates if they’d been aware of the revised data on the labor market that came out a couple of days after the latest meeting. “I suspect we could have had rate cuts in June and July,” Bessent said.
“I don’t know what model he’s talking about,” said Jim Bianco, president of Bianco Research and a longtime Fed and Treasury watcher. “There is no model I’m aware of that says it should be that low,” he said of the Fed’s benchmark.
Other gauges of where the Fed should be, such as the Taylor rule, also aren’t arguing that the main rate should be 150 to 175 basis points lower than it is, Bianco said. He added that there have been many instances over the decades of “cajoling Fed chairs,” and they’re “welcome to offer their opinion,” but it shouldn’t change the central bank leader’s opinion.
Bessent repeated on Thursday that, given the context of the weaker jobs figures and not having cut rates the past couple of months, “perhaps a 50-basis-point cut in September was warranted.”
Two Fed district bank presidents said they’re not backing such a move at this point. San Francisco Fed President Mary Daly said in a Wall Street Journal interview Wednesday, “I just don’t see that. I don’t see the need to catch up.” St. Louis President Alberto Musalem said on CNBC on Thursday that a 50 basis-point cut would be “unsupported by the current state of the economy and the outlook for the economy.”
Flatley writes for Bloomberg.
Air Canada suspended all operations Saturday morning after more than 10,000 flight attendants walked off the job over pay and scheduling disputes, prompting the Canadian government to step in.
Minister Patty Hajdu has directed the Canada Industrial Relations Board to impose binding arbitration, extending the existing contract until a new agreement is reached.
“This decision will help make sure that hundreds of thousands of Canadians and visitors to our country are not impacted because of canceled flights.” Hajdu said in a statement Saturday afternoon.
The strike has already upended travel plans worldwide at the height of the summer season.
The airline, Canada’s largest and the country’s flag carrier, estimates that with its roughly 700 daily flights suspended, some 130,000 customers will be impacted each day the walkout continues.
It’s unclear how long the strike will last or when a deal might be reached. Air Canada Chief Operating Officer Mark Nasr warned that even after an agreement, it could take up to a week to fully restart operations.
Air Canada is urging affected customers not to go to the airport unless they have a confirmed ticket on an airline other than Air Canada or Air Canada Rouge. Flights operated by Air Canada Express partners Jazz and PAL airlines are not impacted.
Passengers whose flights are canceled will be notified. Here’s what travelers need to know:
Customers who booked an Air Canada flight on or before Aug. 15 for travel on Saturday or Sunday can cancel for a full refund of the unused portion of their ticket, regardless of fare type, through the company’s website or mobile app.
Travelers may also opt for a travel credit to use toward a future Air Canada booking.
For other travel dates, refundable ticket holders can request a full refund with no fees. Nonrefundable fares can be converted into credit for future travel.
If you forgo a refund, Air Canada said it will attempt to rebook you, including with other carriers.
But the airline — which serves more than 180 airports in Canada, the United States and on six continents — warned that seats are extremely limited during the peak summer season.
“Available capacity on our airline and on other carriers is limited due to the summer travel peak, meaning the possibility of rebooking you within an acceptable timeframe is low,” Air Canada said in a news release on Saturday.
Passengers can also rebook their flights for dates between Aug. 21 and Sept. 12 at no additional cost.
Air Canada is a member of the Star Alliance network, which includes 26 member airlines such as United and Lufthansa. This means travelers on partner airlines operating Air Canada flights could be affected.
United Airlines said in a statement that it is “working with customers to get them to their destinations and have issued a travel waiver to make sure they have the flexibility to manage their travel plans.”
The Port Authority of New York and New Jersey said that it is “fully prepared to support travelers and help minimize disruptions.”
“Airport staff will be on-site to assist passengers, and we are working closely with Air Canada and our terminal partners to ensure necessary resources are in place,” the agency said in a statement ahead of the strike.
The Port Authority advised that travelers check their flight status directly with Air Canada before heading to the airport and allow extra time for travel.
The U.S. Department of Transportation did not issue an official statement on Air Canada’s suspended operations and did not immediately return a request for comment.
Meta is planning its fourth overhaul of artificial intelligence efforts in six months, The Information reported on Friday, citing three people familiar with the matter.
The company is expected to divide its new AI unit, Superintelligence Labs, into four groups: a new “TBD Lab,” short for to be determined; a products team including the Meta AI assistant; an infrastructure team; and the Fundamental AI Research (FAIR) lab focused on long-term research, the report said, citing two people.
Meta did not immediately respond to a request for comment. Reuters could not independently verify the report.
Read More: Love, lies, and AI
As Silicon Valley’s AI contest intensifies, CEO Mark Zuckerberg is going all-in to fast-track work on artificial general intelligence — machines that can outthink humans — and help create new cash flows.
Meta recently reorganized the company’s AI efforts under Superintelligence Labs, a high-stakes push that followed senior staff departures and a poor reception for Meta’s latest open-source Llama 4 model.
The social media giant has tapped US bond giant PIMCO and alternative asset manager Blue Owl Capital (OWL.N), opens new tab to spearhead a $29 billion financing for its data center expansion in rural Louisiana, Reuters reported earlier this month.
Also Read: Leaked Meta document reveals chatbot rules allowing provocative, harmful content
In July, Zuckerberg said Meta would spend hundreds of billions of dollars to build several massive AI data centers.
The company raised the bottom end of its annual capital expenditures forecast by $2 billion, to a range of $66 billion to $72 billion last month.
Rising costs to build out data center infrastructure and employee compensation costs — as Meta has been poaching researchers with mega salaries — would push the 2026 expense growth rate above the pace in 2025, the company has said.
Fernández-Barat, L. et al. Intensive care unit-acquired pneumonia due to Pseudomonas aeruginosa with and without multidrug resistance. J. Infect. 74, 142–152 (2017).
Google Scholar
Rossi, E. et al. Pseudomonas aeruginosa adaptation and evolution in patients with cystic fibrosis. Nat. Rev. Microbiol. 19, 331–342 (2021).
Google Scholar
Wood, S. J., Kuzel, T. M. & Shafikhani, S. H. Pseudomonas aeruginosa: infections, animal modeling, and therapeutics. Cells 12, 199 (2023).
Lorusso, A. B., Carrara, J. A., Barroso, C. D. N., Tuon, F. F. & Faoro, H. Role of efflux pumps on antimicrobial resistance in Pseudomonas aeruginosa. Int. J. Mol. Sci. 23, 15779 (2022).
Organization, W. H. WHO Bacterial Priority Pathogens List, 2024: Bacterial Pathogens of Public Health Importance, to Guide Research, Development and Strategies to Prevent and Control Antimicrobial Resistance. (World Health Organization, 2024).
Tacconelli, E. et al. Discovery, research, and development of new antibiotics: the WHO priority list of antibiotic-resistant bacteria and tuberculosis. Lancet Infect. Dis. 18, 318–327 (2018).
Google Scholar
Yang, J. J., Tsuei, K.-S. C. & Shen, E. P. The role of type III secretion system in the pathogenesis of Pseudomonas aeruginosa microbial keratitis. Tzu Chi Med. J. 34, 8–14 (2022).
Google Scholar
Muggeo, A., Coraux, C. & Guillard, T. Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium. PLoS Pathog. 19, e1011221 (2023).
Google Scholar
Notti, R. Q. & Stebbins, C. E. The structure and function of type III secretion systems. Microbiol. Spectr. 4, 1–30 (2016).
Yahr, T. L. & Wolfgang, M. C. Transcriptional regulation of the Pseudomonas aeruginosa type III secretion system. Mol. Microbiol. 62, 631–640 (2006).
Google Scholar
Urbanowski, M. L., Lykken, G. L. & Yahr, T. L. A secreted regulatory protein couples transcription to the secretory activity of the Pseudomonas aeruginosa type III secretion system. Proc. Natl Acad. Sci. USA 102, 9930–9935 (2005).
Google Scholar
Vakulskas, C. A., Brady, K. M. & Yahr, T. L. Mechanism of Transcriptional Activation by Pseudomonas aeruginosa ExsA. J. Bacteriol. 191, 6654–6664 (2009).
Google Scholar
McCaw, M. L., Lykken, G. L., Singh, P. K. & Yahr, T. L. ExsD is a negative regulator of the Pseudomonas aeruginosa type III secretion regulon. Mol. Microbiol. 46, 1123–1133 (2002).
Google Scholar
Wagner, S. et al. Bacterial type III secretion systems: a complex device for the delivery of bacterial effector proteins into eukaryotic host cells. FEMS Microbiol. Lett. 365, fny201 (2018).
Forsberg, Å, Viitanen, A.-M., Skurnik, M. & Wolf-Watz, H. The surface-located YopN protein is involved in calcium signal transduction in Yersinia pseudotuberculosis. Mol. Microbiol. 5, 977–986 (1991).
Google Scholar
Joseph, S. S. & Plano, G. V. The SycN/YscB chaperone-binding domain of YopN is required for the calcium-dependent regulation of Yop secretion by Yersinia pestis. Front. Cell Infect. Microbiol. 3, 1 (2013).
Ngo, T.-D. et al. The PopN gate-keeper complex acts on the ATPase PscN to regulate the T3SS secretion switch from early to middle substrates in Pseudomonas aeruginosa. J. Mol. Biol. 432, 166690 (2020).
Google Scholar
Horna, G. & Ruiz, J. Type 3 secretion system of Pseudomonas aeruginosa. Microbiol. Res. 246, 126719 (2021).
Google Scholar
Sana, T. G., Berni, B. & Bleves, S. The T6SSs of Pseudomonas aeruginosa strain PAO1 and their effectors: beyond bacterial-cell targeting. Front. Cell Infect. Microbiol. 6, 61 (2016).
Google Scholar
Habich, A. et al. Distribution of the four type VI secretion systems in Pseudomonas aeruginosa and classification of their core and accessory effectors. Nat. Commun. 16, 888 (2025).
Google Scholar
Hood, R. D. et al. A type VI secretion system of Pseudomonas aeruginosa targets a toxin to bacteria. Cell Host Microbe 7, 25–37 (2010).
Google Scholar
Colautti, J., Kelly, S. D. & Whitney, J. C. Specialized killing across the domains of life by the type VI secretion systems of Pseudomonas aeruginosa. Biochem. J. 482, 1–15 (2025).
Google Scholar
Basler, M., Ho, B. T. & Mekalanos, J. J. Tit-for-tat: type VI secretion system counterattack during bacterial cell-cell interactions. Cell 152, 884–894 (2013).
Google Scholar
Chen, L., Zou, Y., She, P. & Wu, Y. Composition, function, and regulation of T6SS in Pseudomonas aeruginosa. Microbiol Res. 172, 19–25 (2015).
Google Scholar
Stolle, A.-S., Meader, B. T., Toska, J. & Mekalanos, J. J. Endogenous membrane stress induces T6SS activity in Pseudomonas aeruginosa. Proc Natl Acad Sci USA 118, e2018365118 (2021).
Nolan, L. M. et al. Identification of Tse8 as a Type VI secretion system toxin from Pseudomonas aeruginosa that targets the bacterial transamidosome to inhibit protein synthesis in prey cells. Nat. Microbiol. 6, 1199–1210 (2021).
Google Scholar
González-Magaña, A. et al. The P. aeruginosa effector Tse5 forms membrane pores disrupting the membrane potential of intoxicated bacteria. Commun. Biol. 5, 1189 (2022).
Google Scholar
Le, N.-H., Pinedo, V., Lopez, J., Cava, F. & Feldman, M. F. Killing of Gram-negative and Gram-positive bacteria by a bifunctional cell wall-targeting T6SS effector. Proc. Natl Acad. Sci. USA 118, e2106555118 (2021).
Pissaridou, P. et al. The Pseudomonas aeruginosa T6SS-VgrG1b spike is topped by a PAAR protein eliciting DNA damage to bacterial competitors. Proc. Natl Acad. Sci. USA 115, 12519–12524 (2018).
Google Scholar
Russell, A. B. et al. Type VI secretion delivers bacteriolytic effectors to target cells. Nature 475, 343–347 (2011).
Google Scholar
Ross, P. et al. Regulation of cellulose synthesis in Acetobacter xylinum by cyclic diguanylic acid. Nature 325, 279–281 (1987).
Hickman, J. W., Tifrea, D. F. & Harwood, C. S. A chemosensory system that regulates biofilm formation through modulation of cyclic diguanylate levels. Proc. Natl Acad. Sci. USA 102, 14422–14427 (2005).
Google Scholar
Ryan, R. P. et al. HD-GYP domain proteins regulate biofilm formation and virulence in Pseudomonas aeruginosa. Environ. Microbiol. 11, 1126–1136 (2009).
Google Scholar
Guttenplan, S. B. & Kearns, D. B. Regulation of flagellar motility during biofilm formation. FEMS Microbiol. Rev. 37, 849–871 (2013).
Google Scholar
Wang, T., Hua, C. & Deng, X. c-di-GMP signaling in Pseudomonas syringae complex. Microbiol. Res. 275, 127445 (2023).
Google Scholar
Hengge, R. Principles of c-di-GMP signalling in bacteria. Nat. Rev. Microbiol. 7, 263–273 (2009).
Google Scholar
Jenal, U. & Malone, J. Mechanisms of cyclic-di-GMP signaling in bacteria. Annu. Rev. Genet. 40, 385–407 (2006).
Google Scholar
Matsuyama, B. Y. et al. Mechanistic insights into c-di-GMP-dependent control of the biofilm regulator FleQ from Pseudomonas aeruginosa. Proc. Natl Acad. Sci. USA 113, E209–E218 (2016).
Google Scholar
Hickman, J. W. & Harwood, C. S. Identification of FleQ from Pseudomonas aeruginosa as a c-di-GMP-responsive transcription factor. Mol. Microbiol. 69, 376–389 (2008).
Google Scholar
O’Connor, J. R., Kuwada, N. J., Huangyutitham, V., Wiggins, P. A. & Harwood, C. S. Surface sensing and lateral subcellular localization of WspA, the receptor in a chemosensory-like system leading to c-di-GMP production. Mol. Microbiol. 86, 720–729 (2012).
Google Scholar
Baraquet, C., Murakami, K., Parsek, M. R. & Harwood, C. S. The FleQ protein from Pseudomonas aeruginosa functions as both a repressor and an activator to control gene expression from the pel operon promoter in response to c-di-GMP. Nucleic Acids Res. 40, 7207–7218 (2012).
Google Scholar
Lee, V. T. et al. A cyclic-di-GMP receptor required for bacterial exopolysaccharide production. Mol. Microbiol. 65, 1474–1484 (2007).
Google Scholar
Gheorghita, A. A., Wozniak, D. J., Parsek, M. R. & Howell, P. L. Pseudomonas aeruginosa biofilm exopolysaccharides: assembly, function, and degradation. FEMS Microbiol. Rev. 47, fuad060 (2023).
Gupta, K., Liao, J., Petrova, O. E., Cherny, K. E. & Sauer, K. Elevated levels of the second messenger c-di-GMP contribute to antimicrobial resistance of Pseudomonas aeruginosa. Mol. Microbiol. 92, 488–506 (2014).
Google Scholar
Ma, G.-L., Chandra, H. & Liang, Z.-X. Taming the flagellar motor of pseudomonads with a nucleotide messenger. Environ. Microbiol. 22, 2496–2513 (2020).
Google Scholar
Roy, A. B., Petrova, O. E. & Sauer, K. The Phosphodiesterase DipA (PA5017) Is Essential for Pseudomonas aeruginosa Biofilm Dispersion. J. Bacteriol. 194, 2904–2915 (2012).
Google Scholar
Furukawa, S., Kuchma, S. L. & O’Toole, G. A. Keeping their options open: acute versus persistent infections. J. Bacteriol. 188, 1211–1217 (2006).
Google Scholar
Ciofu, O., Mandsberg, L. F., Wang, H. & Høiby, N. Phenotypes selected during chronic lung infection in cystic fibrosis patients: implications for the treatment of Pseudomonas aeruginosa biofilm infections. FEMS Immunol. Med. Microbiol. 65, 215–225 (2012).
Google Scholar
Hall, K. M., Pursell, Z. F. & Morici, L. A. The role of the Pseudomonas aeruginosa hypermutator phenotype on the shift from acute to chronic virulence during respiratory infection. Front. Cell Infect. Microbiol. 12, 943346 (2022).
Mikkelsen, H., Sivaneson, M. & Filloux, A. Key two-component regulatory systems that control biofilm formation in Pseudomonas aeruginosa. Environ. Microbiol. 13, 1666–1681 (2011).
Google Scholar
Allsopp, L. P. et al. RsmA and AmrZ orchestrate the assembly of all three type VI secretion systems in Pseudomonas aeruginosa. Proc. Natl Acad. Sci. USA 114, 7707–7712 (2017).
Google Scholar
Mulcahy, H., O’Callaghan, J., O’Grady, E. P., Adams, C. & O’Gara, F. The posttranscriptional regulator RsmA plays a role in the interaction between Pseudomonas aeruginosa and human airway epithelial cells by positively regulating the type III secretion system. Infect. Immun. 74, 3012–3015 (2006).
Google Scholar
Francis, V. I., Stevenson, E. C. & Porter, S. L. Two-component systems required for virulence in Pseudomonas aeruginosa. FEMS Microbiol. Lett. 364, fnx104 (2017).
Broder, U. N., Jaeger, T. & Jenal, U. LadS is a calcium-responsive kinase that induces acute-to-chronic virulence switch in Pseudomonas aeruginosa. Nat. Microbiol. 2, 16184 (2016).
Google Scholar
Arbel-Goren, R., Tal, A. & Stavans, J. Phenotypic noise: effects of post-transcriptional regulatory processes affecting mRNA. Wiley Interdiscip. Rev. RNA 5, 197–207 (2014).
Google Scholar
Vakulskas, C. A., Potts, A. H., Babitzke, P., Ahmer, B. M. M. & Romeo, T. Regulation of bacterial virulence by Csr (Rsm) systems. Microbiol. Mol. Biol. Rev. 79, 193–224 (2015).
Google Scholar
Moscoso, J. A., Mikkelsen, H., Heeb, S., Williams, P. & Filloux, A. The Pseudomonas aeruginosa sensor RetS switches type III and type VI secretion via c-di-GMP signalling. Environ. Microbiol. 13, 3128–3138 (2011).
Google Scholar
Zhou, T. et al. The two-component system FleS/FleR represses H1-T6SS via cyclic di-GMP signaling in Pseudomonas aeruginosa. Appl. Environ. Microbiol. 88, e0165521 (2022).
Google Scholar
Nie, H. et al. Wsp system oppositely modulates antibacterial activity and biofilm formation via FleQ-FleN complex in Pseudomonas putida. Environ. Microbiol. 24, 1543–1559 (2022).
Google Scholar
Lyng, M. & Kovács, Á. T. Microbial ecology: metabolic heterogeneity and the division of labor in multicellular structures. Curr. Biol. 32, R771–R774 (2022).
Google Scholar
Marsden, A. E. et al. Vfr directly activates exsA transcription to regulate expression of the Pseudomonas aeruginosa type III secretion system. J. Bacteriol. 198, 1442–1450 (2016).
Google Scholar
Laventie, B.-J. et al. A surface-induced asymmetric program promotes tissue colonization by Pseudomonas aeruginosa. Cell Host Microbe 25, 140–152.e6 (2019).
Google Scholar
Laventie, B.-J. & Jenal, U. Surface sensing and adaptation in bacteria. Annu. Rev. Microbiol 74, 735–760 (2020).
Google Scholar
Weigel, W. A. & Dersch, P. Phenotypic heterogeneity: a bacterial virulence strategy. Microbes Infect. 20, 570–577 (2018).
Google Scholar
Christen, M. et al. Asymmetrical distribution of the second messenger c-di-GMP upon bacterial cell division. Science 328, 1295–1297 (2010).
Google Scholar
Valentini, M. & Filloux, A. Biofilms and cyclic di-GMP (c-di-GMP) signaling: lessons from Pseudomonas aeruginosa and Other Bacteria. J. Biol. Chem. 291, 12547–12555 (2016).
Google Scholar
Wang, L. et al. A toolbox of FRET-based c-di-GMP biosensors and its FRET-To-Sort application for genome-wide mapping of the second messenger regulatory network. Preprint at https://doi.org/10.1101/2024.08.21.609041 (2024).
Wang, T. et al. Pleiotropic effects of c-di-GMP content in Pseudomonas syringae. Appl. Environ. Microbiol. 85, e00152-19 (2019).
Christen, M. et al. Identification of small-molecule modulators of diguanylate cyclase by FRET-based high-throughput screening. ChemBioChem 20, 394–407 (2019).
Google Scholar
Ko, M. & Park, C. Two novel flagellar components and H-NS are involved in the motor function of Escherichia coli. J. Mol. Biol. 303, 371–382 (2000).
Google Scholar
Diepold, A., Kudryashev, M., Delalez, N. J., Berry, R. M. & Armitage, J. P. Composition, formation, and regulation of the cytosolic C-ring, a dynamic component of the type III secretion injectisome. PLoS Biol. 13, e1002039 (2015).
Google Scholar
Wimmi, S. et al. Cytosolic sorting platform complexes shuttle type III secretion system effectors to the injectisome in Yersinia enterocolitica. Nat. Microbiol. 9, 185–199 (2024).
Google Scholar
Chua, S. L. et al. Dispersed cells represent a distinct stage in the transition from bacterial biofilm to planktonic lifestyles. Nat. Commun. 5, 4462 (2014).
Google Scholar
Liebl, D., Robert-Genthon, M., Job, V., Cogoni, V. & Attrée, I. Baseplate component TssK and spatio-temporal assembly of T6SS in Pseudomonas aeruginosa. Front. Microbiol. 10, 1615 (2019).
Records, A. R. & Gross, D. C. Sensor kinases RetS and LadS regulate Pseudomonas syringae type VI secretion and virulence factors. J. Bacteriol. 192, 3584–3596 (2010).
Google Scholar
Basler, M. & Mekalanos, J. J. Type 6 secretion dynamics within and between bacterial cells. Science 337, 815–815 (2012).
Google Scholar
Baker, A. E. et al. Flagellar stators stimulate c-di-GMP production by Pseudomonas aeruginosa. J. Bacteriol. 201, e00741–18 (2019).
Kulasekara, B. R. et al. c-di-GMP heterogeneity is generated by the chemotaxis machinery to regulate flagellar motility. Elife 2, e01402 (2013).
Kilmury, S. L. N. & Burrows, L. L. The Pseudomonas aeruginosa PilSR two-component system regulates both twitching and swimming motilities. mBio 9, e01310–18 (2018).
Soscia, C., Hachani, A., Bernadac, A., Filloux, A. & Bleves, S. Cross talk between type III secretion and flagellar assembly systems in Pseudomonas aeruginosa. J. Bacteriol. 189, 3124–3132 (2007).
Google Scholar
Oladosu, V. I., Park, S. & Sauer, K. Flip the switch: the role of FleQ in modulating the transition between the free-living and sessile mode of growth in Pseudomonas aeruginosa. J. Bacteriol. 206, e0036523 (2024).
Zhang, X. et al. NrtR mediated regulation of H1-T6SS in Pseudomonas aeruginosa. Microbiol. Spectr. 10, e01858-21 (2022).
Dadashi, M., Chen, L., Nasimian, A., Ghavami, S. & Duan, K. Putative RNA ligase RtcB affects the switch between T6SS and T3SS in Pseudomonas aeruginosa. Int. J. Mol. Sci. 22, 12561 (2021).
Google Scholar
Wimmi, S. et al. Dynamic relocalization of cytosolic type III secretion system components prevents premature protein secretion at low external pH. Nat. Commun. 12, 1625 (2021).
Google Scholar
Almblad, H. et al. Erratum for Almblad et al., the cyclic AMP-Vfr signaling pathway in Pseudomonas aeruginosa is inhibited by cyclic Di-GMP. J. Bacteriol. 197, 2731–2731 (2015).
Google Scholar
Dasgupta, N., Ferrell, E. P., Kanack, K. J., West, S. E. H. & Ramphal, R. fleQ, the gene encoding the major flagellar regulator of Pseudomonas aeruginosa, Is σ 70 dependent and is downregulated by Vfr, a homolog of Escherichia coli Cyclic AMP receptor protein. J. Bacteriol. 184, 5240–5250 (2002).
Google Scholar
Li, Y., Chen, L., Zhang, P., Bhagirath, A. Y. & Duan, K. ClpV3 of the H3-Type VI secretion system (H3-T6SS) affects multiple virulence factors in Pseudomonas aeruginosa. Front. Microbiol. 11, 1096 (2020).
Rietsch, A. & Mekalanos, J. J. Metabolic regulation of type III secretion gene expression in Pseudomonas aeruginosa. Mol. Microbiol. 59, 807–820 (2006).
Google Scholar
Luo, Y. et al. A hierarchical cascade of second messengers regulates Pseudomonas aeruginosa surface behaviors. mBio 6, e02456–14 (2015).
Speare, L., Jackson, A. & Septer, A. N. Calcium promotes T6SS-mediated killing and aggregation between competing symbionts. Microbiol. Spectr. 10, e0139722 (2022).
Lu, D. et al. Structural insights into the T 6 SS effector protein Tse 3 and the Tse 3– Tsi 3 complex from Pseudomonas aeruginosa reveal a calcium-dependent membrane-binding mechanism. Mol. Microbiol. 92, 1092–1112 (2014).
Google Scholar
Li, S. et al. Autoinducer-2 and bile salts induce c-di-GMP synthesis to repress the T3SS via a T3SS chaperone. Nat. Commun. 13, 6684 (2022).
Google Scholar
Belhart, K., Sisti, F., Gestal, M. C. & Fernández, J. Bordetella bronchiseptica diguanylate cyclase BdcB inhibits the type three secretion system and impacts the immune response. Sci. Rep. 13, 7157 (2023).
Google Scholar
Cai, Y. & Webb, J. S. Optimization of nitric oxide donors for investigating biofilm dispersal response in Pseudomonas aeruginosa clinical isolates. Appl. Microbiol. Biotechnol. 104, 8859–8869 (2020).
Google Scholar
Muhl, D. & Filloux, A. Site-directed mutagenesis and gene deletion using reverse genetics. Methods Mol. Biol. 1149, 521–539 (2014).
Schlechter, R. O. et al. Chromatic bacteria—a broad host-range plasmid and chromosomal insertion toolbox for fluorescent protein expression in bacteria. Front. Microbiol. 9, 3052 (2018).
Google Scholar
Chuanchuen, R., Narasaki, C. T. & Schweizer, H. P. Benchtop and microcentrifuge preparation of Pseudomonas aeruginosa competent cells. Biotechniques 33, 760–763 (2002).
Google Scholar
Lampaki, D., Diepold, A. & Glatter, T. In-depth quantitative proteomics analysis of the Pseudomonas aeruginosa secretome. Methods Mol. Biol. 2721, 197–211 (2024).
Demichev, V., Messner, C. B., Vernardis, S. I., Lilley, K. S. & Ralser, M. DIA-NN: neural networks and interference correction enable deep proteome coverage in high throughput. Nat. Methods 17, 41–44 (2020).
Google Scholar
Ahrné, E., Molzahn, L., Glatter, T. & Schmidt, A. Critical assessment of proteome-wide label-free absolute abundance estimation strategies. Proteomics 13, 2567–2578 (2013).
Google Scholar
Glatter, T. et al. Large-scale quantitative assessment of different in-solution protein digestion protocols reveals superior cleavage efficiency of tandem Lys-C/trypsin proteolysis over trypsin digestion. J. Proteome Res. 11, 5145–5156 (2012).
Google Scholar
Skruzny, M., Pohl, E., Gnoth, S., Malengo, G. & Sourjik, V. The protein architecture of the endocytic coat analyzed by FRET microscopy. Mol. Syst. Biol. 16, e9009 (2020).
Yadavalli, S. S. et al. Functional determinants of a small protein controlling a broadly conserved bacterial sensor kinase. J. Bacteriol. 202, e00305–20 (2020).
Roszik, J., Szöllősi, J. & Vereb, G. AccPbFRET: an ImageJ plugin for semi-automatic, fully corrected analysis of acceptor photobleaching FRET images. BMC Bioinformatics 9, 346 (2008).
Coffey, B. M. & Anderson, G. G. Biofilm formation in the 96-well microtiter plate. Methods Mol. Biol. 1149, 631–641 (2014).
Ha, D.-G., Kuchma, S. L. & O’Toole, G. A. Plate-based assay for swimming motility in Pseudomonas aeruginosa. Methods Mol. Biol. 1149, 59–65 (2014).
Colley, B. et al. SiaA/D interconnects c-di-GMP and RsmA signaling to coordinate cellular aggregation of Pseudomonas aeruginosa in response to environmental conditions. Front. Microbiol. 7, 179 (2016).
Brencic, A. & Lory, S. Determination of the regulon and identification of novel mRNA targets of Pseudomonas aeruginosa RsmA. Mol. Microbiol. 72, 612–632 (2009).
Google Scholar
Burrowes, E., Baysse, C., Adams, C. & O’Gara, F. Influence of the regulatory protein RsmA on cellular functions in Pseudomonas aeruginosa PAO1, as revealed by transcriptome analysis. Microbiology 152, 405–418 (2006).
Google Scholar
Chrome is the world’s most popular web browser. But how much longer it belongs to Google is an open question.
A court last year ruled that Google had violated antitrust laws by maintaining a monopoly on internet search. A second ruling in April found Google also monopolized open-web digital ad markets.
The Justice Department asked a judge to force Google to divest its premier web browser to remedy the case. A court is expected to rule on that by the end of this month.
Chrome, a free web browser developed by Google, is an important distribution tool for Google Search and its other services. It also provides insights into users’ search habits and is the most popular web browser on the market.
Being forced to sell Chrome would be an undeniable blow to Google and its parent company, Alphabet Inc. Analysts at Barclays said such an action could be a black swan scenario for Google stock, sparking an estimated 15% to 25% decline.
Google denies it’s a monopoly. It said in a blog post in May that offloading the web browser to another party could render it “obsolete” and “expose billions of people to cyber-attacks.”
Although the judge has not yet decided Chrome’s ultimate fate, competitors are already lining up to gladly take it off Google’s hands.
Search.com, an AI search chat platform, confirmed to Business Insider that it made a $35 billion bid for Chrome this week. JP Morgan and several private equity firms backed the bid.
Search.com is a division of the digital marketing company Public Good, which Ad.com acquired in July. Public Good President Melissa Anderson and Ad.com CEO Danny Bibi told Business Insider they reached out to Google on Wednesday.
“Given the number of worldwide users Chrome has, it’s a really just phenomenal way to scale user adoption,” Anderson said.
The pair said they’re committed to using AI ethically, which means offering its search for free in an effort to make knowledge accessible for all.
They also said Ad.com, founded in 1998, already has a network of clients, so finding potential advertisers wouldn’t be a heavy lift.
Perplexity, an AI search startup, made a $34.5 billion bid for the web browser this week. The company launched an AI-native browser, Comet, in July.
Although the bid is higher than Perplexity’s entire valuation, The Wall Street Journal reported that several investors have agreed to back the potential deal.
Perplexity said it would continue supporting Chromium, Google’s open-source web browser project that’s the foundation of Chrome, as part of the deal, according to the outlet.
The outlet reported that Perplexity would continue to keep Google as the default search engine, but users could change that through settings.
Although OpenAI’s ChatGPT turned it into the leading AI startup in Silicon Valley, the company is a tiny fraction of the size of a Big Tech mammoth like Google.
Purchasing Chrome, however, would help even the playing field.
During Google’s antitrust hearing in April, OpenAI’s head of ChatGPT testified that the company would be interested in acquiring Chrome if Google were forced to divest.
“Yes, we would, as would many other parties,” Nick Turley told the court, according to Bloomberg.
OpenAI CEO Sam Altman also recently said he’d be interested in snapping up Chrome.
“If Chrome is really going to sell, we should take a look at it,” Altman told a group of journalists on Thursday, according to The Verge.
Yahoo, a direct competitor of Google, would also be interested in bidding on Chrome, Bloomberg reported.
Brian Provost, the general manager for Yahoo Search, said Chrome is “arguably the most important strategic player on the web” during a hearing for Google’s antitrust case in April.
“We would be able to pursue it with Apollo,” Provost said, referring to Yahoo’s owner, Apollo Global Management Inc.
OpenAI has faced a lot of backlash from users after shipping its much-anticipated GPT-5 AI model (touted as the smartest AI model ever) with next-gen capabilities across healthcare sectors, coding, and writing.
Multiple users have blatantly expressed their preference for previous models despite the fact that OpenAI had abruptly decided to deprecate them, including GPT-4o. However, the company recently decided to change this by making these models available again for ChatGPT users.
But unlike before, GPT-5’s predecessors will be buried behind a paywall, meaning you’ll need a $20/month ChatGPT Plus subscription to access them. It’s also worth noting that the AI firm has increased the rate limit for ChatGPT-5 Plus amid backlash from users.
We are significantly increasing rate limits for reasoning for ChatGPT Plus users, and all model-class limits will shortly be higher than they were before GPT-5.
Sam Altman, OpenAI CEO
Perhaps more interestingly, OpenAI CEO Sam Altman recently revealed the “heartbreaking” reason why users are hell-bent on sticking to previous models even after GPT-5 shipped. Speaking to Cleo Abram during an episode of the Huge Conversations podcast, the executive indicated:
“Here is the heartbreaking thing. I think it is great that ChatGPT is less of a yes man and gives you more critical feedback. But as we’ve been making those changes and talking to users about it, it’s so sad to hear users say, ‘Please can I have it back? I’ve never had anyone in my life be supportive of me. I never had a parent tell me I was doing a good job.’”
Watch On
So, the ChatGPT maker’s CEO seems to think users are fixated on previous versions of GPT-5, specifically GPT-4o, because they’ve never had anyone support them before, potentially highlighting how emotionally independent some users are to these AI tools.
The executive further disclosed that some users admitted that ChatGPT’s previous model had encouraged them to make positive changes to their lives. “I can get why this was bad for other people’s mental health, but this was great for my mental health,” Altman echoed some sentiments shared by some users about the model change.
As you may remember, OpenAI rolled out a new update for ChatGPT in April, which seemingly made the tool “overly flattering and agreeable,” prompting some users to suggest that it was exhibiting sycophantic tendencies. Consequently, OpenAI decided to roll back the update. Sam Altman admitted that the update had made ChatGPT’s user experience “too sycophant-y and annoying.”
Admittedly, ChatGPT ships with a handful of helpful features designed to make work easier and can even help people navigate day-to-day life experiences. More recently, OpenAI CEO Sam Altman openly admitted that he was worried about the youth’s emotional over-reliance on ChatGPT:
“People rely on ChatGPT too much. There’s young people who say things like, ‘I can’t make any decision in my life without telling ChatGPT everything that’s going on. It knows me, it knows my friends. I’m gonna do whatever it says.’ That feels really bad to me.”
“Something about collectively deciding we’re going to live our lives the way AI tells us feels bad and dangerous,” added Altman. In a separate report, Sam raised concerns about the high degree of trust people have in ChatGPT despite its tendencies to hallucinate and outrightly generate inaccurate responses to queries. “It should be the tech that you don’t trust that much,” he added.
Elsewhere, the executive indicated that ChatGPT is a better therapist than most professionals in the field across the world, but revealed that he wouldn’t trust the tool with his medical fate unless a medical doctor is in the fold to oversee the process.
Earlier this year, a study by Microsoft revealed that an overreliance on AI tools like ChatGPT and Copilot could make you dumber by atrophying critical thinking, which leads to the deterioration of your cognitive faculties.