Plant growth inhibitory lactones fromPodocarpus neriifolius: Structure of podolactone E

Résumé Le Podolactone E, qui a la structure (4), empêche très activement la croissance des cellules végétales. C'est le plus actif des podolactones isolés jusqu'à présent.     

Side-chain hydroxylation in the biosynthesis of β-ecdysone (20-hydroxyecdysone) in the blowflyCalliphora stygia

Résumé Dans la mouche a viandeCalliphora stygia le 25-hydroxycholesterol et le (22R)-22-hydroxycholesterol sont incorporés a la -ecdysone (20-hydroxy-ecdysone) beaucoup moins qu'au cholesterol et ne sont donc probablement pas des précurseurs de cette hormone.     

The role of crustecdysone in the moulting crayfish

Résumé La crustecdysone injectée dans l'écrevisse,Procambarus sinulans ne cause pas la mue chez l'animal intact mais l'accélère après ablation des pédoncules oculaires.     

Tumour evolution inferred by single-cell sequencing

Genomic analysis provides insights into the role of copy number variation in disease, but most methods are not designed to resolve mixed populations of cells. In tumours, where genetic heterogeneity is common, very important information may be lost that would be useful for reconstructing evolutionary history. Here we show that with flow-sorted nuclei, whole genome amplification and next generation sequencing we can accurately quantify genomic copy number within an individual nucleus. We apply single-nucleus sequencing to investigate tumour population structure and evolution in two human breast cancer cases. Analysis of 100 single cells from a polygenomic tumour revealed three distinct clonal subpopulations that probably represent sequential clonal expansions. Additional analysis of 100 single cells from a monogenomic primary tumour and its liver metastasis indicated that a single clonal expansion formed the primary tumour and seeded the metastasis. In both primary tumours, we also identified an unexpectedly abundant subpopulation of genetically diverse 'pseudodiploid' cells that do not travel to the metastatic site. In contrast to gradual models of tumour progression, our data indicate that tumours grow by punctuated clonal expansions with few persistent intermediates.     

Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas

To identify somatic mutations in pediatric diffuse intrinsic pontine glioma (DIPG), we performed whole-genome sequencing of DNA from seven DIPGs and matched germline tissue and targeted sequencing of an additional 43 DIPGs and 36 non-brainstem pediatric glioblastomas (non-BS-PGs). We found that 78% of DIPGs and 22% of non-BS-PGs contained a mutation in H3F3A, encoding histone H3.3, or in the related HIST1H3B, encoding histone H3.1, that caused a p.Lys27Met amino acid substitution in each protein. An additional 14% of non-BS-PGs had somatic mutations in H3F3A causing a p.Gly34Arg alteration.