Staple, Feasting, or Fallback Food? Mussel Harvesting among Hunter-Gatherers in Interior Central California

Shells are a visible component of archaeological middens in Central California. While coastal and bay shore sites are often dominated by shells, these food items were sometimes hauled many kilometers from their collection points and are found in appreciable numbers in inland sites as well. Using oxygen and carbon stable isotope data from 44 Mytilus sp. (mussel) shells, we reconstruct shellfish seasonality harvesting at one inland site dating to the Middle Period (ca. 2500-1000 cal yrs BP), CA-SOL-364. Data show that shells were collected from nearby Suisun Marsh and were harvested almost exclusively during winter, a pattern that contrasts with coastal and bay shore sites. Such a harvesting signature is unlike that expected for a food staple or a feasting resource. We suggest mussels were harvested as a fallback food, as a source of protein or micronutrient to complement carbohydrate-rich foods that were stored and consumed during winter, or perhaps were only exploited as opportunity costs relaxed during winter, making sessile mussels an attractive subsistence pursuit

Genome-wide mapping of DNA-binding sites identifies stemness-related genes as directly repressed targets of SNAIL1 in colorectal cancer cells

At the molecular level, epithelial-to-mesenchymal transition (EMT) necessitates extensive transcriptional reprogramming which is orchestrated by a small group of gene-regulatory factors that include the zinc-finger DNA-binding protein SNAIL1. Although SNAIL1 is a well-known master regulator of EMT, knowledge of its immediate target genes is incomplete. Here, we used ChIP-seq to identify genes directly regulated by SNAIL1 in colorectal adenocarcinoma cells. When comparing the genomic distribution of SNAIL1 to that of the intestinal stem cell (ISC) transcription factors ASCL2 and TCF7L2, we observed a significant overlap. Furthermore, SNAIL1 ChIP-seq peaks are associated with a substantial fraction of ISC signature genes. In two colorectal cancer cell lines, we verified that SNAIL1 decreases ISC marker expression. Likewise, SNAIL1 directly represses the proto-oncogene MYB, and the long noncoding RNA (lncRNA) WiNTRLINC1, a recently described regulator of ASCL2. SNAIL1 targets multiple regulatory elements at the MYB and WiNTRLINC1 loci, and displaces ASCL2 and TCF7L2 from their binding regions at a MYB downstream regulatory element. Correlation analyses and expression profiling showed antiparallel expression of SNAIL1 and MYB in colorectal and breast cancer cell lines and tumor transcriptomes, suggesting that SNAIL1 controls MYB expression in different tissues. MYB loss-of-function attenuated proliferation and impaired clonogenicity in two- and three-dimensional cell cultures. Therefore, SNAIL1-mediated downregulation of MYB and ISC markers like WiNTRLINC1 likely contributes to the decrease in proliferation known to be associated with EMT, while simultaneously abrogating stemness features of colorectal cancer cells. Apparently, the relationship between EMT and stemness varies in different tumor entities