Alveolar epithelial type 1 (AT1) cells are necessary to transfer oxygen and carbon dioxide between the blood and air. Alveolar epithelial type 2 (AT2) cells serve as a partially committed stem cell population, producing AT1 cells during postnatal alveolar development and repair after influenza A and SARS-CoV-2 pneumonia1–6. Little is known about the metabolic regulation of the fate of lung epithelial cells. Here we report that deleting the mitochondrial electron transport chain complex I subunit Ndufs2 in lung epithelial cells during mouse gestation led to death during postnatal alveolar development. Affected mice displayed hypertrophic cells with AT2 and AT1 cell features, known as transitional cells. Mammalian mitochondrial complex I, comprising 45 subunits, regenerates NAD+ and pumps protons. Conditional expression of yeast NADH dehydrogenase (NDI1) protein that regenerates NAD+ without proton pumping7,8 was sufficient to correct abnormal alveolar development and avert lethality. Single-cell RNA sequencing revealed enrichment of integrated stress response (ISR) genes in transitional cells. Administering an ISR inhibitor9,10 or NAD+ precursor reduced ISR gene signatures in epithelial cells and partially rescued lethality in the absence of mitochondrial complex I function. Notably, lung epithelial-specific loss of mitochondrial electron transport chain complex II subunit Sdhd, which maintains NAD+ regeneration, did not trigger high ISR activation or lethality. These findings highlight an unanticipated requirement for mitochondrial complex I-dependent NAD+ regeneration in directing cell fate during postnatal alveolar development by preventing pathological ISR induction.

1D perovskite materials are of significant interest to build a new class of nanostructures for electronic and optoelectronic applications. However, the study of colloidal perovskite nanowires (PNWs) lags far behind those of other established perovskite materials such as perovskite quantum dots and perovskite thin films. Herein, a dual‐phase passivation strategy to synthesize all‐inorganic PNWs with minimized surface defects is reported. The local phase transition from CsPbBr3 to CsPb2Br5 in PNWs increases the photoluminescence quantum yield, carrier lifetime, and water‐resistivity, owing to the energetic and chemical passivation effect. In addition, these dual‐phase PNWs are employed as an interfacial layer in perovskite solar cells (PSCs). The enhanced surface passivation results in an efficient carrier transfer in PSCs, which is a critical enabler to increase the power conversion efficiency (PCE) to 22.87%, while the device without PNWs exhibits a PCE of 20.74%. The proposed strategy provides a surface passivation platform in 1D perovskites, which can lead to the development of novel nanostructures for future optoelectronic devices.

Indium phosphide (InP) colloidal quantum dots (CQDs) have generated great interest as next-generation light-emitting materials owing to their narrow emission spectra and environment-friendly components. The minimized surface defects is essential to achieve narrow full-width at half-maximum (FWHM) and high photoluminescence quantum yield (PLQY). However, InP CQDs are readily oxidized in ambient condition, which results in formation of oxidation defect states on the surface of InP CQDs. Herein, we introduce a strategy to successfully passivate the surface defects of InP core by zinc complexes. The zinc carboxylates passivation reduces FWHM of InP CQDs from 130 nm to 70 nm and increases PLQY from 1% to 14% without shelling. Furthermore, the photoluminescence (PL) peak has shifted from 670 nm to 510 nm with an increase of zinc carboxylates passivation, which suggests that excessive zinc carboxylates functions as a size-regulating reagent in the synthesis.

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