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Crofts, A. A.

Publications and source records attributed to Crofts, A. A..

2 recordsLinked to original sources

Intrinsic timekeeping in Escherichia coli

Circadian clocks allow organisms to anticipate predictable environmental changes across the day-night cycle. Here we show that the bacterium Escherichia coli exhibits intrinsic timekeeping that anticipates daily temperature cycles. E. coli biofilms entrained to daily temperature shifts, producing 24-hour rhythms in curli plaque formation that persisted under constant temperature. Mechanistically, genetic analyses localized the autonomous timing machinery to the Rcs phosphorelay, which exhibits structural and conceptual parallels with other circadian systems. The BluFR sensory pathway, which acts upstream of the Rcs phosphorelay, linked temperature and blue-light cycles to rhythmic curli production. Flagellar promoter activity and curli production peaked at opposite times of day, suggesting daily coordination of adhesion and motility programs. These findings identify an intrinsic timing system in E. coli that expands our understanding of biological timekeeping.

microbiology↗

Macrophages regulate gastrointestinal motility through complement component 1q

Peristaltic movement of the intestine propels food down the length of the gastrointestinal tract to promote nutrient absorption. Interactions between intestinal macrophages and the enteric nervous system regulate gastrointestinal motility, yet we have an incomplete understanding of the molecular mediators of this crosstalk. Here we identify complement component 1q (C1q) as a macrophage product that regulates gut motility. Macrophages were the predominant source of C1q in the mouse intestine and most extraintestinal tissues. Although C1q mediates complement-mediated killing of bacteria in the bloodstream, we found that C1q was not essential for immune defense of the intestine. Instead, C1q-expressing macrophages were localized to the intestinal submucosal plexus where they closely associated with enteric neurons and expressed surface markers characteristic of nerve-adjacent macrophages in other tissues. Mice with a macrophage-specific deletion of C1qa showed changes in enteric neuronal gene expression, increased peristaltic activity, and accelerated intestinal transit. Our findings identify C1q as a key regulator of gastrointestinal motility and provide enhanced insight into the crosstalk between macrophages and the enteric nervous system.

immunology↗