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Biology subjects

Brownell, D.

Publications and source records attributed to Brownell, D..

2 recordsLinked to original sources

Single-cell, spatial, and fate-mapping analyses uncover niche dependent diversity of cochlear myeloid cells.

Recent advances in fate mapping and single-cell technologies have revealed how the dynamics and function of tissue-resident macrophages are shaped by their environment. However, macrophages in sensory organs such as the cochlea where the central nervous system and peripheral nervous system meet remain understudied. Combining single-cell transcriptomics, fate mapping, and parabiosis experiments, we show that five types of myeloid cells including three tissue-resident macrophage subpopulations, coexist in the mouse cochlea. The three macrophage subsets showed different potential functions in relationship with their specific topography across cochlear compartments. Further analysis revealed that they were partially derived from yolk sac progenitors during development, while in adulthood, most cochlear macrophages were long-term resident. Finally, we showed that cochlear macrophage morphology and density changed during aging. Our findings show that cochlea is a microenvironment with a unique heterogeneity of macrophages in terms of gene expression, spatial distribution, ontogeny, and function.

immunology↗

Alpha-synuclein regulates nucleolar DNA double-strand break repair in melanoma

Although an increased risk of the skin cancer melanoma in people with Parkinsons Disease (PD) has been shown in multiple studies, the mechanisms involved are poorly understood, but increased expression of the PD-associated protein alpha-synuclein (Syn) in melanoma cells may be important. Our previous work suggests that Syn can facilitate DNA double-strand break (DSB) repair, promoting genomic stability. We now show that Syn is preferentially enriched within the nucleolus in the SK-MEL28 melanoma cell line, where it colocalizes with DNA damage markers and DSBs. Inducing DSBs specifically within nucleolar ribosomal DNA (rDNA) increases Syn levels near sites of damage. Syn knockout increases DNA damage within the nucleolus at baseline, after specific rDNA DSB induction, and prolongs the rate of recovery from this induced damage. Syn is important downstream of ATM signaling to facilitate 53BP1 recruitment to DSBs, reducing micronuclei formation and promoting cellular proliferation, migration, and invasion.

cell biology↗