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Gonzalez, D. V.

Publications and source records attributed to Gonzalez, D. V..

2 recordsLinked to original sources

SOX2 can associate with chromatin directly by binding to DNA or indirectly via association with other chromatin-bound proteins

It is widely assumed that SOX2 regulates gene expression and facilitates the opening of chromatin by binding directly at SOX motifs. To test this assumption, we created a SOX2 DNA binding mutant to determine whether other regions of SOX2 contribute to gene target specificity. When exogenously expressed in cells, this SOX2 mutant [SOX2(G76P)], like elevated unmodified SOX2, dramatically alters the transcriptome, but it does so by regulating vastly different gene sets and gene networks than SOX2. Consistent with their differential effects on the transcriptome, ChIP-seq analysis demonstrates that SOX2 and SOX2(G76P) associate primarily with different genomic loci, and motif analysis indicates that SOX2 binds primarily at SOX motifs, whereas SOX2(G76P) associates with chromatin at non-SOX motifs, including AP-1 motifs. Additionally, ATAC-seq analysis indicates that SOX2 substantially increases chromatin accessibility, but SOX2(G76P) does not. The findings presented lead to the conclusion that SOX2(G76P) associates with chromatin indirectly by a "piggyback" mechanism through its association with other chromatin-associated proteins, including AP-1 complexes. Remarkably, we also show that SOX2 and SOX2(G76P) each associate with a subset of the same gene loci that contain several different DNA motifs, including AP-1 motifs, but no high confidence SOX motifs. Overall, our findings provide new perspectives on SOX2 and lead to two important conclusions: 1) selection of gene targets by SOX2 is not solely determined by its DNA binding domain, and 2) SOX2 not only associates with chromatin directly by binding to SOX motifs but can also associate with a subset of gene loci indirectly through its association with other chromatin-associated proteins.

molecular biology↗

Reducing Cholesterol in Resting Macrophage Activates NF-kB through Mitochondria, Resulting in Epigenomic Reprogramming to Dampen Inflammation in Activated Macrophages

Cholesterol plays an important role in macrophage functions including their immune response1. Recently, NF-kB was shown to reprogram the epigenome in macrophages2. Here, we show that NF-kB pathway is activated in resting macrophages when cholesterol is reduced by statin or methyl-{beta}-cyclodextrin (MCD). Activated NF-kB increases the expression of histone-modifying enzymes, such as demethylase JMJD3. We provide evidence that the epigenome in these macrophages is reprogrammed, likely driven by NF-kB and histone modifications2. We also show that cholesterol reduction in macrophages results in suppression of mitochondria respiration. Specifically, cholesterol levels in the inner membrane of the mitochondria is reduced, which impairs the efficiency of ATP synthase (complex V). Consequently, protons accumulate in the intermembrane space to active NF-kB and JMJD3, thereby modifying the epigenome. When subsequently challenged by the inflammatory stimulus lipopolysaccharide (LPS), cholesterol-reduced macrophages generate responses that are less pro-inflammatory and more homeostatic, which should favour inflammation resolution. Taken together, we describe a mechanism by which the level of mitochondrial cholesterol in resting macrophages regulates the epigenome through NF-kB, thereby preparing macrophage for future immune activation.

cell biology↗