Shotgun metagenomics reveals the interplay between microbiome diversity and environmental gradients in the first marine protected area in the northern Arabian Gulf.

Introduction: The northwest Arabian Gulf encounters significant anthropogenic pressures, including nutrient enrichment from coastal development and effluent discharge.

Methods: This study presents the first shotgun metagenomics-based characterization of microbial communities in Kuwaiti waters of the northwest Arabian Gulf, focusing on Kuwait's first Marine Protected Area (MPA) in Sulaibikhat Bay, a vital nursery ground for commercially important fish.

Results: Analysis revealed significantly higher microbial diversity within the MPA compared to adjacent waters, with Rhodobacteraceae (27.

Diversity and spatiotemporal variations in bacterial and archaeal communities within Kuwaiti territorial waters of the Northwest Arabian Gulf.

Kuwaiti territorial waters of the northwest Arabian Gulf represent a unique aquatic ecosystem prone to various environmental and anthropogenic stressors that pose significant constraints on the resident biota which must withstand extreme temperatures, salinity levels, and reducing conditions, among other factors to survive. Such conditions create the ideal environment for investigations into novel functional genetic adaptations of resident organisms. Firstly, however, it is essential to identify said organisms and understand the dynamic nature of their existence.

Enhanced Ribonucleoprotein Immunoprecipitation (RIP) Technique for the Identification of mRNA Species in Ribonucleoprotein Complexes.

RNA binding proteins (RBPs) are critical regulators of cellular phenotypes, and dysregulated RBP expression is implicated in various diseases including cancer. A single RBP can bind to and regulate the expression of many RNA molecules via a variety of mechanisms, including translational suppression, prevention of RNA degradation, and alteration in subcellular localization. To elucidate the role of a specific RBP within a given cellular context, it is essential to first identify the group of RNA molecules to which it binds.

Predicting and explaining the impact of genetic disruptions and interactions on organismal viability.

Motivation: Existing computational models can predict single- and double-mutant fitness but they do have limitations. First, they are often tested via evaluation metrics that are inappropriate for imbalanced datasets. Second, all of them only predict a binary outcome (viable or not, and negatively interacting or not).

Enhanced immunoprecipitation techniques for the identification of RNA-binding protein partners: IGF2BP1 interactions in mammary epithelial cells.

RNA-binding proteins (RBPs) regulate the expression of large cohorts of RNA species to produce programmatic changes in cellular phenotypes. To describe the function of RBPs within a cell, it is key to identify their mRNA-binding partners. This is often done by crosslinking nucleic acids to RBPs, followed by chemical release of the nucleic acid fragments for analysis.

Enhancing Research and Development in the Health Sciences as a Strategy to Establish a Knowledge-Based Economy in the State of Kuwait: A Call for Action.

Kuwait Vision 2035 is an initiative that was launched in 2017 by His Highness the Emir of the State of Kuwait Sheikh Sabah Al-Ahmad Al-Jaber Al-Sabah. This initiative includes the implementation of a detailed development plan aimed at transforming the state of Kuwait into a regional leader in science, technology, and innovation. Health research will arguably prove to be one of the most impactful research arenas when it comes to accomplishing the goals set forth by the Kuwait Vision 2035 Development Plan.

Antiestrogen Therapy Increases Plasticity and Cancer Stemness of Prolactin-Induced ERα Mammary Carcinomas.

Although antiestrogen therapies are successful in many patients with estrogen receptor alpha-positive (ERα) breast cancer, 25% to 40% fail to respond. Although multiple mechanisms underlie evasion of these treatments, including tumor heterogeneity and drug-resistant cancer stem cells (CSC), further investigations have been limited by the paucity of preclinical ERα tumor models. Here, we examined a mouse model of prolactin-induced aggressive ERα breast cancer, which mimics the epidemiologic link between prolactin exposure and increased risk for metastatic ERα tumors.

Lrp5 Has a Wnt-Independent Role in Glucose Uptake and Growth for Mammary Epithelial Cells.

Lrp5 is typically described as a Wnt signaling receptor, albeit a less effective Wnt signaling receptor than the better-studied sister isoform, Lrp6. Here we show that Lrp5 is only a minor player in the response to Wnt3a-type ligands in mammary epithelial cells; instead, Lrp5 is required for glucose uptake, and glucose uptake regulates the growth rate of mammary epithelial cells in culture. Thus, a loss of Lrp5 leads to profound growth suppression, whether growth is induced by serum or by specific growth factors, and this inhibition is not due to a loss of Wnt signaling.

Two Isoforms of the RNA Binding Protein, Coding Region Determinant-binding Protein (CRD-BP/IGF2BP1), Are Expressed in Breast Epithelium and Support Clonogenic Growth of Breast Tumor Cells.

CRD-BP/IGF2BP1 has been characterized as an "oncofetal" RNA binding protein typically highly expressed in embryonic tissues, suppressed in normal adult tissues, but induced in many tumor types. In this study, we show that adult breast tissues express ubiquitous but low levels of CRD-BP protein and mRNA. Although CRD-BP mRNA expression is induced in breast tumor cells, levels remain ∼1000-fold lower than in embryonic tissues.

Wnt signaling in mammary glands: plastic cell fates and combinatorial signaling.

The mouse mammary gland is an outstanding developmental model that exemplifies the activities of many of the effector pathways known to organize mammalian morphogenesis; furthermore, there are well-characterized methods for the specific genetic manipulation of various mammary epithelial cell components. Among these signaling pathways, Wnt signaling has been shown to generate plasticity of fate determination, expanding the genetic programs available to cells in the mammary lineage. It is responsible first for the appearance of the mammary fate in embryonic ectoderm and then for maintaining bi-potential basal stem cells in adult mammary ductal trees.

Both LRP5 and LRP6 receptors are required to respond to physiological Wnt ligands in mammary epithelial cells and fibroblasts.

A canonical Wnt signal maintains adult mammary ductal stem cell activity, and this signal requires the Wnt signaling reception, LRP5. However, previous data from our laboratory have shown that LRP5 and LRP6 are co-expressed in mammary basal cells and that LRP6 is active, leading us to question why LRP6 is insufficient to mediate canonical signaling in the absence of LRP5. Here, we show that at endogenous levels of LRP5 and LRP6 both receptors are required to signal in response to some Wnt ligands both in vitro (in mouse embryonic fibroblasts and mammary epithelial cells) and in vivo (in mammary outgrowths).

p53 null fluorescent yellow direct repeat (FYDR) mice have normal levels of homologous recombination.

The tumor suppressor p53 is a transcription factor whose function is critical for maintaining genomic stability in mammalian cells. In response to DNA damage, p53 initiates a signaling cascade that results in cell cycle arrest, DNA repair or, if the damage is severe, programmed cell death. In addition, p53 interacts with repair proteins involved in homologous recombination.