Stem cells often rely on signals from a niche, which in many tissues adopts a precise morphology. What remains elusive is how niches are formed and how morphology impacts function. To address this, we leverage the Drosophila gonadal niche, which affords genetic tractability and live-imaging. We have previously shown mechanisms dictating niche cell migration to their appropriate position within the gonad and the resultant consequences on niche function. Here, we show that once positioned, niche cells robustly polarize filamentous actin (F-actin) and non-muscle myosin II (MyoII) toward neighboring germ cells. Actomyosin tension along the niche periphery generates a highly reproducible smoothened contour. Without contractility, niches are misshapen and exhibit defects in their ability to regulate germline stem cell behavior. We additionally show that germ cells aid in polarizing MyoII within niche cells and that extrinsic input is required for niche morphogenesis and function. Our work reveals a feedback mechanism where stem cells shape the niche that guides their behavior.

Periphytic algal colonization is common in aquatic systems, but its interspecific competition remains poorly understood. In order to fill the gap, the process of periphytic algal colonization in the Middle Route of the South to North Water Diversion Project was studied. The results showed that the process was divided into three stages: the initial colonization stage (T1, 3-6 days), community formation stage (T2, 12-18 days) and primary succession stage (T3, 24-27 days). In T1, the dominant species were Diatoma vulgaris (Bory), Navicula phyllepta (Kützing) and Fragilaria amphicephaloides (Lange-Bertalot) belonging to Heterokontophyta; these species boasted wide niche widths (NWs), low niche overlap (NO) and low ecological response rates (ERRs). In T2, the dominant species were Diatoma vulgaris, Cymbella affinis (Kützing), Navicula phyllepta, Fragilaria amphicephaloides, Gogorevia exilis (Kützing), Melosira varians (C.Agardh), Phormidium willei (N.L.Gardner) and Cladophora rivularis (Kuntze). These species displayed wider NWs, lower NO, and lower ERRs than those in T1. In T3, the dominant species were Diatoma vulgaris, Cymbella affinis, Navicula phyllepta, Fragilaria amphicephaloides, Achnanthes exigu (Grunow), etc. Among them, Heterokontophyta such as Diatoma vulgaris and Cymbella affinis had a competitive advantage based on NWs and ERRs. Cyanobacteria like Phormidium willei lost their dominant status due to the narrower NW and the increased NO. It could be concluded the interspecific competition became fiercer and shaped the colonization process; this study will be helpful in understanding the colonization of periphytic algal communities.

Unlike sessile macrophages that occupy specialized tissue niches, non-classical monocytes (NCMs)-circulating phagocytes that patrol and cleanse the luminal surface of the vascular tree-are characterized by constant movement. Here, we examined the nature of the NCM\'s nurturing niche. Expression of the growth factor CSF1 on endothelial cells was required for survival of NCMs in the bloodstream. Lack of endothelial-derived CSF1 did not affect blood CSF1 concentration, suggesting that NCMs rely on scavenging CSF1 present on endothelial cells. Deletion of the transmembrane chemokine and adhesion factor CX3CL1 on endothelial cells impaired NCM survival. Mechanistically, endothelial-derived CX3CL1 and integrin subunit alpha L (ITGAL) facilitated the uptake of CSF1 by NCMs. CSF1 was produced by all tissular endothelial cells, and deletion of Csf1 in all endothelial cells except bone marrow sinusoids impaired NCM survival, arguing for a model where the full vascular tree acts as a niche for NCMs and where survival and patrolling function are connected.

Ageing and fertility are intertwined. Germline loss extends the lifespan in various organisms, termed gonadal longevity. However, the original longevity signal from the somatic gonad remains poorly understood. Here, we focused on the interaction between germline stem cells (GSCs) and their niche, the distal tip cells (DTCs), to explore the barely known longevity signal from the somatic gonad in C. elegans. We found that removing germline disrupts the cell adhesions between GSC and DTC, causing a significant transcriptomic change in DTC through hmp-2/β-catenin and two GATA transcription factors, elt-3 and pqm-1 in this niche cell. Inhibiting elt-3 and pqm-1 in DTC suppresses gonadal longevity. Moreover, we further identified the TGF-β ligand, tig-2, as the cytokine from DTC upon the loss of germline, which evokes the downstream gonadal longevity signalling throughout the body. Our findings thus reveal the source of the longevity signalling in response to germline removal, highlighting the stem cell niche as a critical signalling hub in ageing.

Skeletal muscle is one of the tissues with the highest ability to regenerate, a finely controlled process which is critically depending on muscle stem cells. Muscle stem cell functionality depends on intrinsic signaling pathways and interaction with their immediate niche. Upon injury quiescent muscle stem cells get activated, proliferate and fuse to form new myofibers, a process involving the interaction of multiple cell types in regenerating skeletal muscle. Receptors in muscle stem cells receive the respective signals through direct cell-cell interaction, signaling via secreted factors or cell-matrix interactions thereby regulating responses of muscle stem cells to external stimuli. Here, we discuss how muscle stem cells interact with their immediate niche focusing on how this controls their quiescence, activation and self-renewal and how these processes are altered in age and disease.

OBJECTIVE: Women undergoing IVF who have had a previous c-section (CS) have a lower live birth rate than those with a previous vaginal delivery. However, the precise underlying mechanisms need clarification. Does a previous CS affect the pattern of uterine contractility?.
METHODS: Prospective evaluation in patients undergoing frozen blastocyst embryo transfer in medicated endometrial preparation cycles. Twenty patients were included in groups: A/nulliparous. B/previous vaginal delivery. C/ previous CS without a niche, whereas fifteen patients were recruited in group D (CS and a niche). Patients employed estradiol compounds and 800 mg vaginal progesterone. A 3D-scan was performed the transfer-day where uterine contractility/minute was recorded.
RESULTS: Baseline characteristics (age, BMI, smoking, endometrial thickness) were similar. Mean frequency of uterine contractions/minute was similar between groups (1.15, 1.01, 0.92, and 1.21 for groups A, B, C, and D, respectively). There was a slight increase in the number of contractions in patients with a sonographic niche versus controls, not reaching statistical significance (p=0.48). No differences were observed when comparing patients with a previous C-section (regardless of the presence of a niche) to those without a C-section, either nulliparous (p=0.78) or with a previous vaginal delivery (p=0.80). The frequency of uterine contractions was similar between patients who achieved a clinical pregnancy and those who did not (1.19 vs. 1.02 UC/min, p=0.219, respectively).
CONCLUSIONS: Our study found no significant difference in the frequency of uterine contractility between patients with or without a previous C-section or sonographic diagnosed niche. Further investigation is necessary to understand the physiological mechanisms affecting implantation in patients with isthmocele.

Approximately 60% of patients undergoing Cesarean sections may develop Cesarean Scar Defect (CSD), presenting a significant clinical challenge amidst the increasing Cesarean section rates. This condition, marked by a notch in the anterior uterine wall, has evolved as a notable topic in gynecological research. The multifactorial origins of CSD can be broadly classified into labor-related factors, patients\' physical conditions, and surgical quality. However, conflicting influences of certain factors across studies make it challenging to determine effective preventive strategies. Additionally, CSD manifests with diverse symptoms, such as abnormal uterine bleeding, dysmenorrhea, chronic pelvic pain, dyspareunia, secondary infertility, and Cesarean scar pregnancy. Some symptoms are often attributed to other diagnoses, leading to delayed treatment. The quandary of when and how to manage CSD also adds to the complexity. Despite the development of various therapies, clear indications and optimal methods for specific conditions remain elusive. This longstanding challenge has troubled clinicians in both identifying and addressing this iatrogenic disease. Recent studies have yielded some compelling consensuses on various aspects of CSD. This review aims to consolidate the current literature on every facet of CSD. We hope to raise awareness among clinicians about this clinical problem, encouraging more relevant research to unveil the complete picture of CSD.

Early B cell factor 1 (EBF1) is a transcription factor expressed by multiple lineages of stromal cells within the bone marrow. While cultures of Ebf1-deficient cells have been demonstrated to have impaired differentiation into either the osteoblast or adipogenic lineage in vitro by several groups, in vivo there has been a nominal consequence of the loss of EBF1 on skeletal development. In this study we used Prx-cre driven deletion of Ebf1 to eliminate EBF1 from the entire mesenchymal lineage of the skeleton and resolve this discrepancy. We report here that EBF1 is expressed primarily in the Mesenchymal Stem and Progenitor Cell (MSPC)-Adipo, MSPC-Osteo, and the Early Mesenchymal Progenitors, and that loss of EBF1 has a plethora of consequences to maintenance of the skeleton throughout adulthood. Stroma from the Prx-cre;Ebf1fl/fl bones had impaired osteogenic differentiation, an age-dependent loss of CFU-F, and elevated senescence accompanying Ebf1-deletion. New bone formation was reduced after 3 months, and resulted in a quiescent bone environment with fewer osteoblasts and an accompanied reduction in osteoclast-mediated remodeling. Consequently, bones were less ductile at a younger age, and deletion of EBF1 dramatically impaired fracture repair. Disruption of EBF1 in perivascular populations also rearranged the vascular network within these bones and disrupted cytokine signaling from key hematopoietic niches resulting in anemia, reductions in B cells, and myeloid skewing of marrow hematopoietic lineages. Mechanistically we observed disrupted BMP signaling within Ebf1-deficient progenitors with reduced SMAD1-phosphorylation, and elevated secretion of the soluble BMP-inhibitor Gremlin from the MSPC-Adipo cells. Ebf1-deficient progenitors also exhibited posttranslational suppression of glucocorticoid receptor expression. Together, these results suggest that EBF1 signaling is required for mesenchymal progenitor mobilization to maintain the adult skeleton, and that the primary action of EBF1 in the early mesenchymal lineage is to promote proliferation, and differentiation of these perivascular cells to sustain a healthy tissue.

Extensive research has explored the functional correlation between stem cells and progenitor cells, particularly in blood. Hematopoietic stem cells (HSCs) can self-renew and regenerate tissues within the bone marrow, while stromal cells regulate tissue function. Recent studies have validated the role of mammalian stem cells within specific environments, providing initial empirical proof of this functional phenomenon. The interaction between bone and blood has always been vital to the function of the human body. It was initially proposed that during evolution, mammalian stem cells formed a complex relationship with the surrounding microenvironment, known as the niche. Researchers are currently debating the significance of molecular-level data to identify individual stromal cell types due to incomplete stromal cell mapping. Obtaining these data can help determine the specific activities of HSCs in bone marrow. This review summarizes key topics from previous studies on HSCs and their environment, discussing current and developing concepts related to HSCs and their niche in the bone marrow.

Tumorigenesis is a complicated process in which numerous modulators are involved in different ways. Previous studies have focused primarily on tumor-associated protein-coding genes such as oncogenes and tumor suppressor genes, as well as their associated oncogenic pathways. However, noncoding RNAs (ncRNAs), rising stars in diverse physiological and pathological processes, have recently emerged as additional modulators in tumorigenesis. In this review, we focus on two typical kinds of ncRNAs: long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs). We describe the molecular patterns of ncRNAs and focus on the roles of ncRNAs in cancer stem cells (CSCs), tumor cells, and tumor environmental cells. CSCs are a small subset of tumor cells and are generally considered to be cells that initiate tumorigenesis, and dozens of ncRNAs have been defined as critical modulators in CSC maintenance and oncogenesis. Moreover, ncRNAs are widely involved in oncogenetic processes, including sustaining proliferation, resisting cell death, genome instability, metabolic disorders, immune escape and metastasis. We also discuss the potential applications of ncRNAs in tumor diagnosis and therapy. The progress in ncRNA research greatly improves our understanding of ncRNAs in oncogenesis and provides new potential targets for future tumor therapy.