Local environment shapes milk microbiomes while evolutionary history constrains milk macronutrients in captive cercopithecine primates.

Milk is a complex biochemical fluid that includes macronutrients and microbiota, which, together, are known to facilitate infant growth, mediate the colonization of infant microbiomes, and promote immune development. Examining factors that shape milk microbiomes and milk-nutrient interplay across host taxa is critical to resolving the evolution of the milk environment. Using a comparative approach across four cercopithecine primate species housed at three facilities under similar management conditions, we test for the respective influences of the local environment (housing facility) and host species on milk (a) macronutrients (fat, sugar, and protein), (b) microbiomes (16S rRNA), and (c) predicted microbial functions. We found that milk macronutrients were structured according to host species, while milk microbiomes and predicted function were strongly shaped by the local environment and, to a lesser extent, host species. The milk microbiomes of rhesus macaques (Macaca mulatta) at two different facilities more closely resembled those of heterospecific facility-mates compared to conspecifics at a different facility. We found similar, facility-driven patterns of microbial functions linked to physiology and immune modulation, suggesting that milk microbiomes may influence infant health and development. These results provide novel insight into the complexity of milk and its potential impact on infants across species and environments.

The chromatin remodeling protein CHD-1 and the EFL-1/DPL-1 transcription factor cooperatively down regulate CDK-2 to control SAS-6 levels and centriole number.

Centrioles are submicron-scale, barrel-shaped organelles typically found in pairs, and play important roles in ciliogenesis and bipolar spindle assembly. In general, successful execution of centriole-dependent processes is highly reliant on the ability of the cell to stringently control centriole number. This in turn is mainly achieved through the precise duplication of centrioles during each S phase. Aberrations in centriole duplication disrupt spindle assembly and cilia-based signaling and have been linked to cancer, primary microcephaly and a variety of growth disorders. Studies aimed at understanding how centriole duplication is controlled have mainly focused on the post-translational regulation of two key components of this pathway: the master regulatory kinase ZYG-1/Plk4 and the scaffold component SAS-6. In contrast, how transcriptional control mechanisms might contribute to this process have not been well explored. Here we show that the chromatin remodeling protein CHD-1 contributes to the regulation of centriole duplication in the C. elegans embryo. Specifically, we find that loss of CHD-1 or inactivation of its ATPase activity can restore embryonic viability and centriole duplication to a strain expressing insufficient ZYG-1 activity. Interestingly, loss of CHD-1 is associated with increases in the levels of two ZYG-1-binding partners: SPD-2, the centriole receptor for ZYG-1 and SAS-6. Finally, we explore transcriptional regulatory networks governing centriole duplication and find that CHD-1 and a second transcription factor, EFL-1/DPL-1 cooperate to down regulate expression of CDK-2, which in turn promotes SAS-6 protein levels. Disruption of this regulatory network results in the overexpression of SAS-6 and the production of extra centrioles.