Transcriptomics of independent CRISPR-edited cell lines reveal ciliary-specific ARL13B dependent changes

u4atac regulates cilium biogenesis through splicing of the minor intron of tmem107l and rfx7b in zebrafish developing brain

Cbx3a/HP1γ Deficiency Disrupts Meiotic Progression and Triggers Germ Cell Apoptosis in Nile Tilapia

Heterochromatin Protein 1γ, encoded by the Cbx3 gene, is a crucial epigenetic regulator that plays an essential role in mammalian meiotic progression. However, the functional divergence and conservation of this protein in teleosts—organisms possessing duplicated Cbx3 paralogs due to whole-genome duplication—remain to be elucidated. Building on previous research, we focused on cbx3a in Nile tilapia (Oreochromis niloticus), a significant aquaculture species and an excellent model for teleost reproductive studies, emphasizing its role in spermatogenesis. Expression analysis revealed that Cbx3a is localized to primordial germ cells and is sustained in spermatogonia, spermatocytes, and spermatids during spermatogenesis. CRISPR/Cas9-mediated knockout of cbx3a demonstrated that Cbx3a deficiency induces germ cell apoptosis, meiotic arrest, and sperm defects, including shortened tails and impaired motility, resulting in profound defects in sperm quantity and quality, strongly implying compromised male fertility. Transcriptomic analysis further identified dysregulated molecular pathways, including cytokine signaling and neuroactive ligand–receptor interactions. This provides novel mechanistic insights into HP1γ-mediated epigenetic regulation of meiosis. Notably, cbx3a mutants exhibited phenotypic bifurcation: a subset showed meiotic defects accompanied by sporadic germ cell apoptosis, whereas others underwent full meiotic arrest with pervasive germ cell apoptosis in adult gonads. Collectively, these findings clarify the essential and conserved role of Cbx3a/HP1γ in Nile tilapia spermatogenesis, thereby advancing the field of vertebrate reproductive epigenetics and providing a valuable theoretical basis for potential applications in reproductive management, such as improving sperm quality.

Regulation of de- and reciliation by KRAS during muscle cell differentiation

A major mediator of mitogenic signaling into the regulation of ciliogenesis of proliferating muscle stem- and progenitor cells is integrated into the regulation of ciliogenesis of proliferating muscle stem- and progenitor cells.

MS4A8B regulates Orai1-dependent Ca²⁺ influx to control motile cilia function in human nasal epithelial cells

Targeting this compartmentalized signaling pathway offers a novel therapeutic approach to restore or enhance mucociliary clearance in airway diseases.

The minor spliceosome component U4atac regulates JAK/STAT signaling to modulate hematopoiesis and immune responses in Drosophila melanogaster.

It is revealed that mutations in U4atac affect the splicing of a large set of transcripts involved in innate immunity, hematopoiesis, and intestinal cell functions, including the Drosophila Janus kinase (JAK) homolog hopscotch (hop).

Loss of cohesin subunit Stag1 in zebrafish limits cell cycle progression and is compensated by altered BMP signalling and metabolic pathways

Cohesin is a large multisubunit protein complex that plays essential roles in cell proliferation, genome organisation, and gene regulation in metazoans. Germline mutations in cohesin subunits or regulators cause a group of human developmental disorders collectively known as cohesinopathies. Increasing evidence indicates that individual cohesin subunits can confer distinct molecular functions to the complex; for example, STAG1 and STAG2 have both overlapping and non-overlapping roles in genome organisation. The zebrafish tailbud provides an excellent developmental model for investigating the coordination of cell proliferation and differentiation; processes in which cohesin has crucial functions. We previously demonstrated that loss of Stag2 disrupts Wnt signalling and mesoderm patterning in the zebrafish tailbud. Here, we show that, unlike mammals, zebrafish can tolerate complete loss of Stag1 from embryogenesis through to adulthood. In contrast to Stag2 deficiency, loss of Stag1 impairs cell cycle progression, activates p53 signalling, and induces a metabolic shift towards catabolism. BMP signalling is reduced in Stag1-deficient embryos and is accompanied by expansion of BMP antagonist chordin expression. Stag1 loss also alters chromatin accessibility at the chordin locus and affects accessibility at chromatin domain boundaries. We propose that modulation of growth and signalling pathways compensates for the absence of Stag1, allowing embryonic development to proceed correctly. Together, these findings reveal distinct contributions of Stag1 and Stag2 to cell-cycle regulation, chromatin architecture, and developmental signalling during vertebrate embryogenesis.