98%
921
2 minutes
20
Larval settlement is of interest both for ecologists and for evolutionary biologists, who have proposed that anterior sensory systems for substrate selection provided the basis for animal brains. Nevertheless, the cellular and molecular regulation of settlement, including in Cnidaria (corals, jellyfish, sea anemones, and hydroids), is not well understood. We generated and compared anterior (aboral) transcriptomes and single-cell RNA sequencing datasets from the planula larvae of three cnidarian species: the jellyfish and the corals and . Integrating these datasets and characterizing aboral cell types, we defined common cellular features of the planula aboral end and identified clade-specific specializations in cell types. Among shared features were genes implicated in taurine uptake and catabolism expressed in distinct specialized aboral cell types. In functional assays using both and planulae, exogenous taurine inhibited settlement. These findings define the molecular and cellular architecture of the planula aboral pole and implicate localized taurine destruction in regulating settlement.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12225738 | PMC |
http://dx.doi.org/10.1126/sciadv.adv1159 | DOI Listing |
J Am Soc Nephrol
September 2025
Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN, USA.
Background: Genetic modifiers are believed to play an important role in the onset and severity of polycystic kidney disease (PKD), but identifying these modifiers has been challenging due to the lack of effective methodologies.
Methods: We generated zebrafish mutants of IFT140, a skeletal ciliopathy gene and newly identified autosomal dominant PKD (ADPKD) gene, to examine skeletal development and kidney cyst formation in larval and juvenile mutants. Additionally, we utilized ift140 crispants, generated through efficient microhomology-mediated end joining (MMEJ)-based genome editing, to compare phenotypes with mutants and conduct a pilot genetic modifier screen.
J Clin Invest
September 2025
Department of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter, United Kingdom.
Understanding the genetic causes of diseases affecting pancreatic β cells and neurons can give insights into pathways essential for both cell types. Microcephaly, epilepsy and diabetes syndrome (MEDS) is a congenital disorder with two known aetiological genes, IER3IP1 and YIPF5. Both genes encode proteins involved in endoplasmic reticulum (ER) to Golgi trafficking.
View Article and Find Full Text PDFJ Clin Invest
September 2025
Department of Cellular and Molecular Medicine, UCSD, La Jolla, United States of America.
3-O-sulfation of heparan sulfate (HS) is the key determinant for binding and activation of Antithrombin III (AT). This interaction is the basis of heparin treatment to prevent thrombotic events and excess coagulation. Antithrombin-binding HS (HSAT) is expressed in human tissues, but is thought to be expressed in the subendothelial space, mast cells, and follicular fluid.
View Article and Find Full Text PDFRNA Biol
September 2025
Department of Stem Cell Biology, School of Medicine, Konkuk University, Seoul, Republic of Korea.
Neural stem cells (NSCs) are multipotent stem cells with self-renewal capacity, able to differentiate into all neural lineages of the central nervous system, including neurons, oligodendrocytes, and astrocytes; thus, their proliferation and differentiation are essential for embryonic neurodevelopment and adult brain homoeostasis. Dysregulation in these processes is implicated in neurological disorders, highlighting the need to elucidate how NSCs proliferate and differentiate to clarify the mechanisms of neurogenesis and uncover potential therapeutic targets. MicroRNAs (miRNAs) are small, post-transcriptional regulators of gene expression involved in many aspects of nervous system development and function.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2025
School of Medicine, Chongqing University, Chongqing 400044, China.
Engineering functional exosomes represents a cutting-edge approach in biomedicine, holding the promise to transform targeted therapy. However, challenges such as achieving consistent modification and scalability have limited their wider adoption. Herein, we introduce a universal and effective strategy for engineering multifunctional exosomes through cell fusion.
View Article and Find Full Text PDF