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In the human fungal pathogen Cryptococcus neoformans, sex can benefit its pathogenicity through production of meiospores, which are believed to offer both physical and meiosis-created lineage advantages for its infections. Cryptococcus sporulation occurs following two parallel events, meiosis and differentiation of the basidium, the characteristic sexual structure of the basidiomycetes. However, the circuit integrating these events to ensure subsequent sporulation is unclear. Here, we show the spatiotemporal coordination of meiosis and basidial maturation by visualizing event-specific molecules in developing basidia defined by a quantitative approach. Monitoring of gene induction timing together with genetic analysis reveals co-regulation of the coordinated events by a shared regulatory program. Two RRM family regulators, Csa1 and Csa2, are crucial components that bridge meiosis and basidial maturation, further determining sporulation. We propose that the regulatory coordination of meiosis and basidial development serves as a determinant underlying the production of infectious meiospores in C. neoformans. Many microbes that cause disease form spores to survive during and between infections. These include the fungus Cryptococcus neoformans, which is the leading cause of fungal meningitis worldwide. This fungus produces spores via sexual reproduction, meaning the genes from two living strains of the fungi combine to create new lives with unique genetics. By diversifying the fungus’s genetics, sexual reproduction in Cryptococcus is considered to accelerate drug resistance. Several processes must be coordinated for Cryptococcus to reproduce sexually. Genetic information recombines through a process called meiosis, the spore-making cell (known as the sexual structure) matures and later spores are produced. Scientists have identified many genes involved in each of these processes. Yet it is not known how these processes are coordinated to ensure the proper sequence of events. Liu, He, Chen et al. studied the physical changes in Cryptococcus cells when they lost certain genes. Two genes, which the researchers named CSA1 and CSA2, were found to regulate the parallel progression of meiosis and maturation of the sexual structure. Both processes need to be complete before spore production begins. Further investigation showed that these genes are important across various strains of infectious Cryptococcus. This research highlights sexual reproduction as a target to stop Cryptococcus forming spores and starting infections. The results also show that these processes change little through evolution within a large group of fungi. The next step will be to see how these systems operate across species and the effect this has on spore production.

Urbanization is a worldwide phenomenon associated with tremendous modifications of natural habitats. Understanding how city dwelling species are affected by those changes is becoming a pressing issue. We presently lack fine scale spatio-temporal studies investigating the impact of urbanization across different life stages and along urbanization gradients. Based on 8 years of monitoring of urban and forest great tits (Parus major), we investigated how city life shapes morphological characteristics at different life stages in the city versus the forest, and within the urban habitat (along naturalness and pedestrian frequency gradients). We found that urban nestlings were significantly smaller than forest ones, but not in lower body condition. Urban breeders showed reduced tarsus, wing and tail lengths compared to forest birds. Within the city, variation in nestling tarsus length and body condition along the naturalness gradient highly depended on the year, with no consistent pattern. For breeders, tarsus length and body condition were positively correlated to the naturalness gradient, although only in 2019 for tarsus, and only in older individuals for body condition. Finally, we found that males had smaller wing lengths in more urbanized parts of the city. These results suggest that urbanization affects morphology early on in development, influencing many morphological attributes. While the mechanisms underlying the urban morphotype remain to be determined, we discuss the potential origins for the documented differences between forest and urban morphotypes, and argue that they most probably result from urban environmental constraints linked to food availability.