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SummaryIn budding yeast, chitin is found in three locations: at the primary septum, largely in free form, at the mother-bud neck, partially linked to b(1-3)glucan, and in the lateral wall, attached in part to b(1-6)glucan. By using a recently developed strategy for the study of cell wall cross-links, we have found that chitin linked to b(1-6)glucan is diminished in mutants of the CRH1 or the CRH2/UTR2 gene and completely absent in a double mutant. This indicates that Crh1p and Crh2p, homologues of glycosyltransferases, ferry chitin chains from chitin synthase III to b(1-6)glucan. Deletion of CRH1 and/or CRH2 aggravated the defects of fks1D and gas1D mutants, which are impaired in cell wall synthesis. A temperature shift from 30°C to 38°C increased the proportion of chitin attached to b(1-6)glucan. The expression of CRH1, but not that of CRH2, was also higher at 38°C in a manner dependent on the cell integrity pathway. Furthermore, the localization of both Crh1p and Crh2p at the cell cortex, the area where the chitin-b(1-6)glucan complex is found, was greatly enhanced at 38°C. Crh1p and Crh2p are the first proteins directly implicated in the formation of cross-links between cell wall components in fungi.

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We have studied LO phonon-plasmon coupled modes by means of Raman scattering in n-InP for carrier densities between 6ϫ10 16 and 1ϫ10 19 cm Ϫ3 . A line-shape theory based on the Lindhard-Mermin dielectric function that takes into account the nonparabolicity of the InP conduction band as well as temperature and finite wave-vector effects is used to fit the Raman spectra and extract accurate values of the electron density. The results obtained from the Lindhard-Mermin model are compared with the charge density determinations based on the Drude and the hydrodynamical models, and the approximations involved in these models are discussed. ͓S0163-1829͑99͒10431-4͔

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The mitochondrial ATP synthase emerges as key hub of cellular functions controlling the production of ATP, cellular signaling, and fate. It is regulated by the ATPase inhibitory factor 1 (IF1), which is highly abundant in neurons. Herein, we ablated or overexpressed IF1 in mouse neurons to show that IF1 dose defines the fraction of active/inactive enzyme in vivo, thereby controlling mitochondrial function and the production of mitochondrial reactive oxygen species (mtROS). Transcriptomic, proteomic, and metabolomic analyses indicate that IF1 dose regulates mitochondrial metabolism, synaptic function, and cognition. Ablation of IF1 impairs memory, whereas synaptic transmission and learning are enhanced by IF1 overexpression. Mechanistically, quenching the IF1-mediated increase in mtROS production in mice overexpressing IF1 reduces the increased synaptic transmission and obliterates the learning advantage afforded by the higher IF1 content. Overall, IF1 plays a key role in neuronal function by regulating the fraction of ATP synthase responsible for mitohormetic mtROS signaling.

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