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Powers, S.

Publications and source records attributed to Powers, S..

2 recordsLinked to original sources

Single-cell genomic analysis of triple-negative breast cancer fibroblasts uncovers evolutionarily conserved features and potential therapeutic targets

To comprehend cancer-associated fibroblasts (CAFs) origins, single-cell RNA sequencing was conducted on normal and cancerous breast tissue from mice and humans. We found three conserved CAF subtypes, which based on GOterm analysis we designated as matrix CAFs-, chemokine CAFs, and contractile CAFs. Matrix and chemokine CAFs originated from resident fibroblasts, while contractile CAFs originated from normal pericytes. Both human and mouse CAFs displayed upregulated genes involved in extracellular matrix organization, cellular respiration, and cell migration. Key transcription factors in both species included NFKB1, SP1, TP53, and TWIST2. Trajectory inference suggested that in some cases a transitory state characterized by JUN expression precedes the maturation of CAFs. Computational analysis revealed a common mechanism for CAF education involving the overexpression of TGF-{beta}, PDGF, TNF, and NOTCH-family ligands in different tumor microenvironment cell types, along with reciprocal overexpression of receptors in CAFs. These findings bolster and broaden current understandings of CAF genesis.

cancer biology↗

The F-box protein AFF1 regulates ARF protein accumulation to regulate auxin response

Auxin critically regulates nearly every aspect of plant growth and development. Auxin-driven transcriptional responses are mediated through the AUXIN RESPONSE FACTOR (ARF) family of transcription factors. Although ARF protein stability is regulated via the 26S proteasome, molecular mechanisms underlying ARF stability and turnover are unknown. Here, we report the identification and functional characterization of an F-box E3 ubiquitin ligase, which we have named AUXIN RESPONSE FACTOR F-BOX1 (AFF1). AFF1 directly interacts with ARF19 and regulates its accumulation. Mutants defective in AFF1 display ARF19 protein hyperaccumulation, attenuated auxin responsiveness, and developmental defects. Together, our data suggest a new mechanism, namely control of ARF protein stability, in regulating auxin response.

plant biology↗