Diversity of Arbuscular Mycorrhizal Fungi in the Rhizosphere of Solaris and Regent Grapevine Plants Treated with Bioproducts

The aim of this study was to identify the spores of arbuscular mycorrhizal fungi (AMF) in the rhizosphere of Solaris and Regent grapevine plants grafted onto SO4 rootstock and treated with bioproducts. The bioproducts Ausuma, Bioilsa, manure and BF Ekomix were tested and applied on their own, or combined with standard mineral fertilisation (NPK). The applied bioproducts contributed to an increase in the number of species of mycorrhizal fungi in the rhizosphere soil of the grapevines. The most frequently occurring AMF species was Claroideoglomus claroideum. Biopreparation BF Ekomix was a promisingagent for increasing the number of AMF spores in the rhizosphere of Regent grapevines. In the rhizosphere of Solaris, a positive influence on the number of spores occurred after the application of Bioilsa

Mutant p53 as a guardian of the cancer cell

Forty years of research have established that the p53 tumor suppressor provides a major barrier to neoplastic transformation and tumor progression by its unique ability to act as an extremely sensitive collector of stress inputs, and to coordinate a complex framework of diverse effector pathways and processes that protect cellular homeostasis and genome stability. Missense mutations in the TP53 gene are extremely widespread in human cancers and give rise to mutant p53 proteins that lose tumor suppressive activities, and some of which exert trans-dominant repression over the wild-type counterpart. Cancer cells acquire selective advantages by retaining mutant forms of the protein, which radically subvert the nature of the p53 pathway by promoting invasion, metastasis and chemoresistance. In this review, we consider available evidence suggesting that mutant p53 proteins can favor cancer cell survival and tumor progression by acting as homeostatic factors that sense and protect cancer cells from transformation-related stress stimuli, including DNA lesions, oxidative and proteotoxic stress, metabolic inbalance, interaction with the tumor microenvironment, and the immune system. These activities of mutant p53 may explain cancer cell addiction to this particular oncogene, and their study may disclose tumor vulnerabilities and synthetic lethalities that could be exploited for hitting tumors bearing missense TP53 mutations

YAP and β-catenin cooperate to drive oncogenesis in basal breast cancer

Targeting cancer stem cells (CSC) can serve as an effective approach toward limiting resistance to therapies. While basal-like (triple-negative) breast cancers encompass cells with CSC features, rational therapies remain poorly established. We show here that the receptor tyrosine kinase Met promotes YAP activity in basal-like breast cancer and find enhanced YAP activity within the CSC population. Interfering with YAP activity delayed basal-like cancer formation, prevented luminal to basal trans-differentiation, and reduced CSC. YAP knockout mammary glands revealed a decrease in β-catenin target genes, suggesting that YAP is required for nuclear β-catenin activity. Mechanistically, nuclear YAP interacted with β-catenin and TEAD4 at gene regulatory elements. Proteomic patient data revealed an upregulation of the YAP signature in basal-like breast cancers. Our findings demonstrate that in basal-like breast cancers, β-catenin activity is dependent on YAP signalling and controls the CSC program. These findings suggest that targeting the YAP/TEAD4/β-catenin complex offers a potential therapeutic strategy for eradicating CSCs in basal-like breast cancers

Perennial flower strips for pest control in organic apple orchards

Orchards often have low diversity of plant species, which limits the promotion of natural enemies to combat the important apple pests Dysaphis plantaginea (Passerini) and Cydia pomonella (L.). We developed perennial, multifunctional flower strips with native plant species and trialed these in organic apple orchards in seven European countries. On average 73.7% of the sown plant species were established and plant diversity of flower strips was on average 43% higher than the spontaneous orchard vegetation. Intensive mulching of flower strips affected the plant community: species richness and ground cover by forbs and plants, which especially promote functional agrobiodiversity, decreased significantly. Visual assessments over two years revealed a higher number of natural enemies on plant parts, and specifically in D. plantaginea colonies, on trees in flower strip plots than on trees in control plots with standard orchard vegetation. Trees in the flower strip plots recorded a slower D. plantaginea population increase as compared with control plots, resulting in reduced fruit damage after the second fruit drop. Likewise, from 2016–2017, the number of preadult codling moths decreased more in the flower strip plots as compared to the control plots resulting in reduced fruit damage. Our study shows on a wide continental scale that the implementation of perennial flower strips in the alleyways between apple tree rows boosts natural enemies and reduces key apple pests and the associated fruit damage. This supports the role of functional agrobiodiversity as a way to potentially reduce insecticide use in orchards and thus further promote conservation of agrobiodiversity. The project “EcoOrchard” was provided by FP7 ERAnet, CORE Organic Plus and cofinanced by the European Commission

Proteasome machinery is instrumental in a common gain-of-function program of the p53 missense mutants in cancer

In cancer, the tumour suppressor gene TP53 undergoes frequent missense mutations that endow mutant p53 proteins with oncogenic properties. Until now, a universal mutant p53 gain-of-function program has not been defined. By means of multi-omics: proteome, DNA interactome (chromatin immunoprecipitation followed by sequencing) and transcriptome (RNA sequencing/microarray) analyses, we identified the proteasome machinery as a common target of p53 missense mutants. The mutant p53-proteasome axis globally affects protein homeostasis, inhibiting multiple tumour-suppressive pathways, including the anti-oncogenic KSRP-microRNA pathway. In cancer cells, p53 missense mutants cooperate with Nrf2 (NFE2L2) to activate proteasome gene transcription, resulting in resistance to the proteasome inhibitor carfilzomib. Combining the mutant p53-inactivating agent APR-246 (PRIMA-1MET) with the proteasome inhibitor carfilzomib is effective in overcoming chemoresistance in triple-negative breast cancer cells, creating a therapeutic opportunity for treatment of solid tumours and metastasis with mutant p53