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The efficacy of using agar-bound microparticulate diet (A-MPD) as alternative food for abalone Haliotis asinina Linne post-larvae in large-scale culture was investigated. Larvae sourced from the hatchery-bred (HB) and wild-sourced (WS) broodstock were fed with either diatoms (TMT1-NF), agar-bound microparticulate diet (TMT2-A-MPD), or a combination of both feeds (TMT3-NF + A-MPD) in six 2-m tanks replicated over time. Three hundred thousand veliger larvae were stocked/tank containing 80 corrugated plates with mucus trails hanging on bamboo poles. Feeds were given at 0900 h starting at day 3 with seawater flow through introduced every 1400 h starting day 5. Two-way analysis of variance determined significant differences ( p < 0.05) in survival and shell length between larval sources and feed types. Tukey's post hoc test established differences among treatment means. At day 30, survival for HB- and WS-sourced larvae was significantly higher (42%) in TMT3 compared with TMT2 having 35% for HB and 38% for WS ( p < 0.05). Larvae fed with TMT1 had significantly lowest survival among the three treatments. Survival at 60 and 90 days did not show significant difference for TMT2 and TMT3 regardless of broodstock source. Post-larval shell growth (90 days), from both sources fed with TMT2 and TMT3, was significantly higher than TMT1 ( p < 0.05). Larval performance did not show any significant interactions between HB and WS broodstock. The use of A-MPD alone or in combination may elicit improvement in survival and shell length growth in abalone larvae regardless of larval sources. A-MPD may be used as full or partial replacements to diatoms as alternative food for abalone post-larvae in large-scale culture. [ABSTRACT FROM AUTHOR]

In breast cancer, the increased stiffness of the extracellular matrix is a key driver of malignancy. Yet little is known about the epigenomic changes that underlie the tumorigenic impact of extracellular matrix mechanics. Here, we show in a three-dimensional culture model of breast cancer that stiff extracellular matrix induces a tumorigenic phenotype through changes in chromatin state. We found that increased stiffness yielded cells with more wrinkled nuclei and with increased lamina-associated chromatin, that cells cultured in stiff matrices displayed more accessible chromatin sites, which exhibited footprints of Sp1 binding, and that this transcription factor acts along with the histone deacetylases 3 and 8 to regulate the induction of stiffness-mediated tumorigenicity. Just as cell culture on soft environments or in them rather than on tissue-culture plastic better recapitulates the acinar morphology observed in mammary epithelium in vivo, mammary epithelial cells cultured on soft microenvironments or in them also more closely replicate the in vivo chromatin state. Our results emphasize the importance of culture conditions for epigenomic studies, and reveal that chromatin state is a critical mediator of mechanotransduction.