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The chimp was a great start. But the genomes of our other primate relatives will help to reveal a whole lot more, says Carina Dennis., The chimpanzee genome The cover photo by Kevin Langergraber shows the adult female chimpanzee ‘Jolie’ in Kibale National Park, Uganda. This was taken on 16 August 2004, a few weeks before Jolie gave birth to her first infant. This week marks a landmark in the study of our closest living relative: the publication by the Chimpanzee Sequencing and Analysis Consortium of the initial sequence of the chimpanzee genome, together with a comparison with the human genome. The paper describes changes that have shaped human and chimpanzee species since the split from our common ancestor, and hints at what makes us uniquely human: 35 million single-nucleotide substitutions, 5 million small insertions and deletions, local rearrangements and a chromosome fusion. A comparison of gene duplications in chimpanzee and human genomes reveals gene expression differences that may underlie disease susceptibility. A study of primate genomes shows that subtelomeres are hot spots of recent chromosomal duplication and gene conversion. Conservation of Y-linked genes during human evolution is revealed by comparative sequencing in the chimpanzee. The final research paper in this collection fills a big gap in our knowledge: the first chimpanzee fossils ever found show that chimps and early humans inhabited the same environments in which they evolved and diverged. The fossils — three teeth — are from half-million-year-old sediments in Kenya that also yielded fossils of Homo. Four Progress reviews accompany these papers, looking at chimp culture, social behaviour, psychology and cognition. Elsewhere in the issue, researchers talk about working with chimpanzees, a feature summarizes other primate genome projects, and in two Commentaries, important ethical issues surrounding research on great apes are considered.

A list of authors and their affiliations appears at the end of the paper New-particle formation is a major contributor to urban smog1,2, but how it occurs in cities is often puzzling3. If the growth rates of urban particles are similar to those found in cleaner environments (1–10 nanometres per hour), then existing understanding suggests that new urban particles should be rapidly scavenged by the high concentration of pre-existing particles. Here we show, through experiments performed under atmospheric conditions in the CLOUD chamber at CERN, that below about +5 degrees Celsius, nitric acid and ammonia vapours can condense onto freshly nucleated particles as small as a few nanometres in diameter. Moreover, when it is cold enough (below −15 degrees Celsius), nitric acid and ammonia can nucleate directly through an acid–base stabilization mechanism to form ammonium nitrate particles. Given that these vapours are often one thousand times more abundant than sulfuric acid, the resulting particle growth rates can be extremely high, reaching well above 100 nanometres per hour. However, these high growth rates require the gas-particle ammonium nitrate system to be out of equilibrium in order to sustain gas-phase supersaturations. In view of the strong temperature dependence that we measure for the gas-phase supersaturations, we expect such transient conditions to occur in inhomogeneous urban settings, especially in wintertime, driven by vertical mixing and by strong local sources such as traffic. Even though rapid growth from nitric acid and ammonia condensation may last for only a few minutes, it is nonetheless fast enough to shepherd freshly nucleated particles through the smallest size range where they are most vulnerable to scavenging loss, thus greatly increasing their survival probability. We also expect nitric acid and ammonia nucleation and rapid growth to be important in the relatively clean and cold upper free troposphere, where ammonia can be convected from the continental boundary layer and nitric acid is abundant from electrical storms4,5., Measurements in the CLOUD chamber at CERN show that the rapid condensation of ammonia and nitric acid vapours could be important for the formation and survival of new particles in wintertime urban conditions, contributing to urban smog.

A Correction to this paper has been published: https://doi.org/10.1038/s41586-020-03176-6.

Many patients experiencing sudden loss of lung tissue somehow undergo full recovery; here this recovery is traced to a discrete population of lung stem cells that are not only essential for lung regeneration but can be cloned and then transplanted to other mice to contribute new lung tissue. Supplementary information The online version of this article (doi:10.1038/nature13903) contains supplementary material, which is available to authorized users., Stem cells for lung regeneration The extent to which patients can recover after massive loss of lung tissue has been unclear. However, clinical experience has shown that large-scale lung regeneration can occur in children and adults following catastrophic lung damage, and previous studies in mice have linked a subset of cells from distal airway to a regeneration process observed after H1N1 influenza virus mediated injury. Two papers published in this issue show that when the epithelial cells lining the interior of the lung are damaged, a rare stem cell population is induced to proliferate and migrate to the damaged site where they differentiate into several cell types. Frank McKeon and colleagues describe a rare subset of mouse distal airway cells that proliferate after exposure to influenza. These cells can contribute to lung regeneration after transplantation and maintain their intrinsic lineage commitment in cell culture, suggesting that such cell subsets may have potential in stem-cell-based therapies. Harold Chapman and colleagues used lineage tracing to identify a population of quiescent cells in the mouse distal lung that are activated after bleomycin or influenza-mediated injury. These cells express cytokeratin 5 and repair the epithelium through a Notch signalling pathway, although persistent Notch signalling in this context then leads to the formation of cysts. Data from patients suffering from lung fibrosis also show the presence of hyperactive Notch and similar cysts. Supplementary information The online version of this article (doi:10.1038/nature13903) contains supplementary material, which is available to authorized users., Lung diseases such as chronic obstructive pulmonary disease1 and pulmonary fibrosis2 involve the progressive and inexorable destruction of oxygen exchange surfaces and airways, and have emerged as a leading cause of death worldwide. Mitigating therapies, aside from impractical organ transplantation, remain limited and the possibility of regenerative medicine has lacked empirical support. However, it is clinically known that patients who survive sudden, massive loss of lung tissue from necrotizing pneumonia3,4 or acute respiratory distress syndrome5,6 often recover full pulmonary function within six months. Correspondingly, we recently demonstrated lung regeneration in mice following H1N1 influenza virus infection, and linked distal airway stem cells expressing Trp63 (p63) and keratin 5, called DASCp63/Krt5, to this process7. Here we show that pre-existing, intrinsically committed DASCp63/Krt5 undergo a proliferative expansion in response to influenza-induced lung damage, and assemble into nascent alveoli at sites of interstitial lung inflammation. We also show that the selective ablation of DASCp63/Krt5 in vivo prevents this regeneration, leading to pre-fibrotic lesions and deficient oxygen exchange. Finally, we demonstrate that single DASCp63/Krt5-derived pedigrees differentiate to type I and type II pneumocytes as well as bronchiolar secretory cells following transplantation to infected lung and also minimize the structural consequences of endogenous stem cell loss on this process. The ability to propagate these cells in culture while maintaining their intrinsic lineage commitment suggests their potential in stem cell-based therapies for acute and chronic lung diseases. Supplementary information The online version of this article (doi:10.1038/nature13903) contains supplementary material, which is available to authorized users.