Identification and validation of two quantitative trait loci for dwarf bunt in the resistant cultivar 'UI Silver'.

Two dwarf bunt resistance QTLs were mapped to chromosome 6D, and KASP markers associated with the loci were developed and validated in a panel of regionally adapted winter wheats. UI Silver is an invaluable adapted resistant cultivar possessing the two identified QTL potentially associated with genes Bt9 and Bt10 and will be useful in future cultivar development to improve dwarf bunt resistance. Dwarf bunt, caused by Tilletia controversa, is a fungal disease of wheat that can cause complete loss of grain yield and quality during epidemics.

Multiomics reveals age-dependent metabolic reprogramming of macrophages by wound bed niche secreted signals.

Unlabelled: The cellular metabolism of macrophages depends on tissue niches and can control macrophage inflammatory or resolving phenotypes. Yet, the identity of signals within tissue niches that control macrophage metabolism is not well understood. Here, using single-cell RNA sequencing of macrophages in early mouse wounds, we find that, rather than gene expression of canonical inflammatory or resolving polarization markers, metabolic gene expression defines distinct populations of early wound macrophages.

Transcriptional analysis of efferocytosis in mouse skin wounds.

Defects in apoptotic cell clearance, or efferocytosis, can cause inflammatory diseases and prevent tissue repair due in part to inducing a pro-repair transcriptional program in phagocytic cells like macrophages. While the cellular machinery and metabolic pathways involved in efferocytosis have been characterized, the precise efferocytic response of macrophages is dependent on the identity and macromolecular cues of apoptotic cells, and the complex tissue microenvironment in which efferocytosis occurs. Here, we find that macrophages undergoing active efferocytosis in mid-stage mouse skin wounds in vivo display a pro-repair gene program, while efferocytosis of apoptotic skin fibroblasts in vitro also induces an inflammatory transcription response.

A maternal brain hormone that builds bone.

In lactating mothers, the high calcium (Ca) demand for milk production triggers significant bone loss. Although oestrogen normally counteracts excessive bone resorption by promoting bone formation, this sex steroid drops precipitously during this postpartum period. Here we report that brain-derived cellular communication network factor 3 (CCN3) secreted from KISS1 neurons of the arcuate nucleus (ARC) fills this void and functions as a potent osteoanabolic factor to build bone in lactating females.

Apoptosis recognition receptors regulate skin tissue repair in mice.

Apoptosis and clearance of apoptotic cells via efferocytosis are evolutionarily conserved processes that drive tissue repair. However, the mechanisms by which recognition and clearance of apoptotic cells regulate repair are not fully understood. Here, we use single-cell RNA sequencing to provide a map of the cellular dynamics during early inflammation in mouse skin wounds.