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The CRISPR/Cas9 system is unable to edit all targetable genomic sites with full efficiency in vivo. We show that Cas9-mediated editing is more efficient in open chromatin regions than in closed chromatin regions in rice. A construct (Cas9-TV) formed by fusing a synthetic transcription activation domain to Cas9 edits target sites more efficiently, even in closed chromatin regions. Moreover, combining Cas9-TV with a proximally binding dead sgRNA (dsgRNA) further improves editing efficiency up to several folds. The use of Cas9-TV/dsgRNA thus provides a novel strategy for obtaining efficient genome editing in vivo, especially at nuclease-refractory target sites. Electronic supplementary material The online version of this article (10.1186/s13059-019-1762-8) contains supplementary material, which is available to authorized users.

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Surfactin produced by Bacillus subtilis is a powerful biosurfactant in food, cosmetics, and pesticide industries. However, its suitability in wound healing applications is uncertain. In this article, we determined the effects of surfactin A from B. subtilis on wound healing, angiogenesis, cell migration, inflammatory response, and scar formation. The results indicated that 80.65 ± 2.03% of surfactin A-treated wounds were closed, whereas 44.30 ± 4.26% of the vehicle-treated wound areas remained open on day 7 (P < 0.05). In mechanisms, it upregulated the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF), accelerated keratinocyte migration through mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signaling pathways, and regulated the secretion of proinflammatory cytokines and macrophage phenotypic switch. More attractive, surfactin A showed a seductive capability to inhibit scar tissue formation by affecting the expression of α-smooth muscle actin (α-SMA) and transforming growth factor (TGF-β). Overall, the study revealed a new function and potential of surfactin A as an affordable and efficient wound healing drug.

Lactobacillus rhamnosus SHA113 showed therapic effects on the instestinal infection caused by Staphylococcus aureus, especially multi-drug-resistant (MDR) pathogenic S. aureus.