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Golder, C.

Publications and source records attributed to Golder, C..

2 recordsLinked to original sources

Stress triggers global histone synthesis in the liver

Despite extensive drug development targeting DNA synthesis, there have been few efforts to inhibit histone synthesis, which occurs jointly with DNA synthesis in S-phase. A major roadblock is the lack of tools to quantitatively measure histone synthesis due to the high abundance and stability of histone proteins. Here we present chemical labeling methodologies to produce the first in vivo measurements of histone synthesis rates. Under basal conditions, histone synthesis tracks closely with tissue proliferation. However, multiple systemic and liver-specific stresses induce a previously uncharacterized surge of hepatocyte nucleosome production that is uncoupled from DNA replication. Tracing of newly synthesized nucleosomes detected promoter deposition, which was required to buffer transcriptional output. These results may inform strategies to modulate histone production to influence stress responses or disease.

molecular biology↗

VISTA-induced tumor suppression by a four amino acid intracellular motif

VISTA is a key immune checkpoint receptor under investigation for cancer immunotherapy; however, its signaling mechanisms remain unclear. Here we identify a conserved four amino acid (NPGF) intracellular motif in VISTA that suppresses cell proliferation by constraining cell-intrinsic growth receptor signaling. The NPGF motif binds to the adapter protein NUMB and recruits Rab11 endosomal recycling machinery. We identify and characterize a class of triple-negative breast cancers with high VISTA expression and low proliferative index. In tumor cells with high VISTA levels, the NPGF motif sequesters NUMB at endosomes, which interferes with epidermal growth factor receptor (EGFR) trafficking and signaling to suppress tumor growth. These effects do not require canonical VISTA ligands, nor a functioning immune system. As a consequence of VISTA expression, EGFR receptor remains abnormally phosphorylated and cannot propagate ligand-induced signaling. Mutation of the VISTA NPGF domain reverts VISTA-induced growth suppression in multiple breast cancer mouse models. These results define a mechanism by which VISTA represses NUMB to control malignant epithelial cell growth and signaling. They also define distinct intracellular residues that are critical for VISTA-induced cell-intrinsic signaling that could be exploited to improve immunotherapy.

cancer biology↗