Combined application of arbuscular mycorrhizae fungi and plant growth promoting bacteria improves growth and nutrient uptake efficiency of pea (Pisum sativum L.) plants

The study aimed to investigate the effects of commercially available AMF inoculate (a mixture of Rhizophagus intraradices, Claroideoglomus etunicatum, Funneliformis mossea, Funneliformis geosporum, Rhizophagus clarus) and plant growth promoting bacteria (Rhizobium leguminosarum and Burkholderia sp.), either supplied individually or in combination with each other, on growth, root morphology and nutrient uptake capabilities in field pea (Pisum sativum L.) plants. Inoculated and non-inoculated pea plants were subjected to three levels of salinity (0, 20 and 50 mM) by the addition of sodium chloride into tap water. Morphology of root system was analyzed and dry matter of roots and shoots were individually measured several times during the growing cycle in randomly selected plants. The dry matter of roots and shoots was mixed together and concentration of N, P, K and Na was analytically determined. The raise of salinity in the irrigation water has strongly diminished the growth of pea plants by significantly reducing the weight, length, and surface area of root system, and deteriorating its nutrient capabilities. The inoculation of either AM fungi or PGPB in the growing substrate has contributed to alleviating the salinity stress effects through promoting growth and enhancing nutrient uptake capabilities of the root system. The combined application of AM fungi and PGPB could further enhance the nutrient uptake capabilities of pea plants under adverse salinity conditions

THE EFFECTS OF ROOT INTERVENTION ON STAND ESTABLISHMENT RATE OF GRAFTED WATERMELON (CITRULLUS AEDULIS L) SEEDLINGS UNDER SALINE CONDITIONS

Abstract A commercial watermelon (Citrullus aedulis L) variety was grafted onto a commercial variety rootstock (Cucurbita maxima x C. moschata ). Two different grafting methods; splice grafting (SG) and root pruned splice grafting (RPSG) were simultaneously applied. End of nursery period, a sufficient number of 14 day old seedlings of each grafting method were transplanted in large pots filled with a mixture of peat compost and vermiculite (3:1). The plants were split in three equal groups and in the following 14 days each group was periodically irrigated with equal amounts of respectively tap water or saline water (50 mM NaCl and 100 mM NaCL). The relative growth rate (RGR) and its components; net assimilation rate (NAR) and leaf area ratio (LAR), root relative growth rate (RRGR), stem elongation rate (SER) and leaf expansion relative rate (LER) were computed for each experimental plot. Additionally to that, equal weights of fresh roots from seedlings of both grafting methods were washed out carefully with tap water and immersed into equal quantities of methanol. Several diluted solutions (10% vol/vol, 15% vol/vol and 20% vol/vol) were prepared from each root extracts, parallel with control solutions (0.01, 0.05 and 0.1 ppm) of artificial cytokinins, and used as rooting medium for 20 day old cuttings of tepary bean (Phaseoulus acutifolius). The average number of root nodes and lateral roots as well as the average length of lateral roots of tepary bean cuttings was used to indicate the difference between RPSG and SG seedlings regarding the nature and quantity of growth hormones extracted from the fresh rootstock roots. A significantly higher relative growth rate was found for root pruned splice grafted seedlings after transplanting, mostly due to higher net assimilation rate, as well as a higher root relative growth rate indicating a faster stand establishment rate for RPSG seedlings. Generally speaking, the relative growth rate of transplanted seedlings was drastically reduced due to the increase of nutrient solution salinity. However, significantly higher values were recorded for root pruned splice grafted seedlings compared to splice grafted ones. The same was true regarding root relative growth rate, stem elongation rate and leaf expansion rate. A higher concentration of cytokinins, was indicated by a higher rooting index of Phaseoulus acutifolius, from the extracts of RPSG seedlings and to that is attributed their significantly higher stand establishment rate

Cotton row spacing and plant density cropping systems I. Effects on accumulation and partitioning of dry mass and LAI

Increase of plant density with decreasing cotton row spacing has been suggested as an alternative strategy to optimize cotton profit. Although, the primary goal of this method is to reduce input cost, however, there is limited information about the agronomic and physiological aspects of these systems across the world cotton belt. In this task, three cultivation systems were studied in terms of narrow row high plant density (NRHPD; 48 cm and 32 plants/m(2)), narrow row low plant density (NRLPD; 48 cm and 16 plants/m(2)) and conventional row spacing (CR; 96 cm and 16 plants/m(2)). Effects of these systems on the accumulation and allocation of dry mass as well as on leaf area index (LAI) were examined at critical growth stages during two growing seasons. Independently of row spacing, system with high plant density (NRHPD) produced significantly (P <= 0.001) greater dry mass and leaf area index (LAI) compared to lower plant density systems, i.e. CR and NRLPD. These differences became more significant at stage of maximum dry mass and LAI. However, this system of NRHPD partitioned the same or less dry mass to reproductive growth than other systems. Also, significant (P <= 0.05) differences were measured between systems with the same plant density and different row spacing, thus total dry mass and LAI were significantly higher in NRLPD than in CR system

PI3K Inhibition Activates SGK1 via a Feedback Loop to Promote Chromatin-Based Regulation of ER-Dependent Gene Expression

Summary: The PI3K pathway integrates extracellular stimuli to phosphorylate effectors such as AKT and serum-and-glucocorticoid-regulated kinase (SGK1). We have previously reported that the PI3K pathway regulates estrogen receptor (ER)-dependent transcription in breast cancer through the phosphorylation of the lysine methyltransferase KMT2D by AKT. Here, we show that PI3Kα inhibition, via a negative-feedback loop, activates SGK1 to promote chromatin-based regulation of ER-dependent transcription. PI3K/AKT inhibitors activate ER, which promotes SGK1 transcription through direct binding to its promoter. Elevated SGK1, in turn, phosphorylates KMT2D, suppressing its function, leading to a loss of methylation of lysine 4 on histone H3 (H3K4) and a repressive chromatin state at ER loci to attenuate ER activity. Thus, SGK1 regulates the chromatin landscape and ER-dependent transcription via the direct phosphorylation of KMT2D. These findings reveal an ER-SGK1-KMT2D signaling circuit aimed to attenuate ER response through a role for SGK1 to program chromatin and ER transcriptional output. : Toska, Castel, et al. show that the PI3K pathway propagates its effects to control chromatin and estrogen receptor (ER) function through SGK1, a PI3K effector. PI3K inhibitors, via a negative-feedback loop, activate SGK1, which phosphorylates the histone lysine methyltransferase KMT2D to attenuate its activity and regulate ER response. Keywords: SGK1, KMT2D, PI3K pathway, estrogen receptor, breast cancer, chromatin regulation, AKT, PI3K inhibitor

The Oncogenic PI3K-Induced Transcriptomic Landscape Reveals Key Functions in Splicing and Gene Expression Regulation

The phosphoinositide 3-kinase (PI3K) pathway regulates proliferation, survival, and metabolism and is frequently activated across human cancers. A comprehensive elucidation of how this signaling pathway controls transcriptional and cotranscriptional processes could provide new insights into the key functions of PI3K signaling in cancer. Here, we undertook a transcriptomic approach to investigate genome-wide gene expression and transcription factor activity changes, as well as splicing and isoform usage dynamics, downstream of PI3K. These analyses uncovered widespread alternatively spliced isoforms linked to proliferation, metabolism, and splicing in PIK3CA-mutant cells, which were reversed by inhibition of PI3Kα. Analysis of paired tumor biopsies from patients with PIK3CA-mutated breast cancer undergoing treatment with PI3Kα inhibitors identified widespread splicing alterations that affect specific isoforms in common with the preclinical models, and these alterations, namely PTK2/FRNK and AFMID isoforms, were validated as functional drivers of cancer cell growth or migration. Mechanistically, isoform-specific splicing factors mediated PI3K-dependent RNA splicing. Treatment with splicing inhibitors rendered breast cancer cells more sensitive to the PI3Kα inhibitor alpelisib, resulting in greater growth inhibition than alpelisib alone. This study provides the first comprehensive analysis of widespread splicing alterations driven by oncogenic PI3K in breast cancer. The atlas of PI3K-mediated splicing programs establishes a key role for the PI3K pathway in regulating splicing, opening new avenues for exploiting PI3K signaling as a therapeutic vulnerability in breast cancer. Transcriptomic analysis reveals a key role for the PI3K pathway in regulating RNA splicing, uncovering new mechanisms by which PI3K regulates proliferation and metabolism in breast cancer. See related commentary by Claridge and Hopkins, p. 2216

ARID1A determines luminal identity and therapeutic response in estrogen-receptor-positive breast cancer

Mutations in ARID1A, a subunit of the SWI/SNF chromatin remodeling complex, are the most common alterations of the SWI/SNF complex in estrogen-receptor-positive (ER+) breast cancer. We identify that ARID1A inactivating mutations are present at a high frequency in advanced endocrine-resistant ER+ breast cancer. An epigenome CRISPR–CAS9 knockout (KO) screen identifies ARID1A as the top candidate whose loss determines resistance to the ER degrader fulvestrant. ARID1A inactivation in cells and in patients leads to resistance to ER degraders by facilitating a switch from ER-dependent luminal cells to ER-independent basal-like cells. Cellular plasticity is mediated by loss of ARID1A-dependent SWI/SNF complex targeting to genomic sites of the luminal lineage-determining transcription factors including ER, forkhead box protein A1 (FOXA1) and GATA-binding factor 3 (GATA3). ARID1A also regulates genome-wide ER–FOXA1 chromatin interactions and ER-dependent transcription. Altogether, we uncover a critical role for ARID1A in maintaining luminal cell identity and endocrine therapeutic response in ER+ breast cancer