Dissected Leaf 1 encodes an MYB transcription factor that controls leaf morphology in potato.

KEY MESSAGE: The transcription factor StDL1 regulates dissected leaf formation in potato and the genotype frequency of recessive Stdl1/Stdl1, which results in non-dissected leaves, has increased in cultivated potatoes. Leaf morphology is a key trait of plants, influencing plant architecture, photosynthetic efficiency and yield. Potato (Solanum tuberosum L.), the third most important food crop worldwide, has a diverse leaf morphology. However, despite the recent identification of several genes regulating leaf formation in other plants, few genes involved in potato leaf development have been reported. In this study, we identified an R2R3 MYB transcription factor, Dissected Leaf 1 (StDL1), regulating dissected leaf formation in potato. A naturally occurring allele of this gene, Stdl1, confers non-dissected leaves in young seedlings. Knockout of StDL1 in a diploid potato changes the leaf morphology from dissected to non-dissected. Experiments in N. benthamiana and yeast show that StDL1 is a transcriptional activator. Notably, by calculating the genotype frequency of the Stdl1/Stdl1 in 373-potato accessions, we found that it increases significantly in cultivated potatoes. This work reveals the genetic basis of dissected leaf formation in potato and provides insights into plant leaf morphology.

Multi-parametric cellular imaging coupled with multi-component quantitative profiling for screening of hepatotoxic equivalent markers from Psoraleae Fructus.

BACKGROUND: The hepatotoxicity of Chinese herbal medicine (CHM) is an important reason for its restrictive application. Psoraleae Fructus (PF), a commonly used CHM for treatment of osteoporosis and vitiligo etc., has caused serious concern due to the frequent occurrence of liver injury incidents. To date, its hepatotoxic equivalent markers (HEMs) and potential mechanisms are still unclear. PURPOSE: To discover and validate the HEMs of PF and further explore the potential mechanisms of hepatotoxicity. METHODS: Multi-parametric cellular imaging was performed by high content screening, and multi-component quantitative profiling was conducted by ultra-high performance liquid chromatography coupled with triple-quadrupole mass spectrometry. The correlations between hepatotoxic features and component contents were modeled by chemometrics including partial least square regression, back propagation-artificial neural network, and hierarchical cluster analysis. Then the candidate HEMs of PF were screened out and subjected to hepatotoxic equivalence assessment in primary hepatocytes, zebrafish, and mice, and the hepatotoxic mechanisms of PF were investigated. RESULTS: The chemical combination of psoralen and isopsoralen was discovered as the HEMs of PF through pre-screening and verifying process. PF was demonstrated to induce oxidative stress, mitochondrial dysfunction and cellular apoptosis. CONCLUSIONS: This study not only provides a rational strategy for screening HEMs from CHMs like PF, but also contributes to understanding the underlying mechanisms of PF hepatotoxicity.