Genes to Cells最新文献

Long noncoding RNAs (lncRNAs) are abundantly transcribed in eukaryotes, but most of their physiological roles, especially in neural development, remain unclear due to limited in vivo studies. Here we show that Lobe-less (LOL) lncRNA of Drosophila is expressed in developing neuronal cells and is required for the development of the mushroom body, a center of memory and learning in the insect brain. lol mutant flies exhibit defective morphology of the mushroom body and axon branch patterns, as well as misregulation of neurogenic genes. LOL RNA forms nuclear puncta and genetically interacts with Polycomb group genes in the regulation of homeotic genes. These findings demonstrate that this long ncRNA plays a critical role in the epigenetic control of neural circuit formation.

The 7th International Conference on Plant Vascular Biology 2025 (PVB2025) took place at the KKR Hotel Osaka from July 7th to July 12th. The conference attracted 169 participants from 20 countries, including 105 attendees from outside Japan. PVB2025 featured 12 plenary scientific sessions, 23 invited talks, 31 contributed talks selected from submitted abstracts, and 89 poster presentations. Plant vascular biology is a crucial area of plant science, as vascular systems transport essential resources that plants need for survival. These systems also function as a communication network, facilitating internal and external information flow at the whole-body level. Participants at PVB2025 aimed to share their latest findings in this field. Additionally, the conference emphasized the importance of inspiring and encouraging young scientists who will become the next generation of community leaders. To support this initiative, we offered five travel awards and five Best Poster Awards to undergraduate students, graduate students, and early-career professionals. Overall, PVB2025 successfully fostered discussions and collaborations in plant vascular biology research while allowing participants to experience the unique and vibrant culture of Osaka through “eating and talking till you drop.”

Hepatic peroxisome proliferator-activated receptor gamma (PPARγ) promotes fat accumulation in the liver of leptin-deficient (ob/ob) mice. However, the mechanism underlying PPARγ-dependent fat accumulation remains unclear. In this study, we identified miR-205-5p as a liver-enriched microRNA regulated by PPARγ. miR-205-5p was significantly upregulated in the ob/ob mouse livers and induced by treatment with the PPARγ-specific agonist rosiglitazone. In contrast, its expression was markedly reduced in liver-specific PPARγ knockout mice. In both nonalcoholic fatty liver and nonalcoholic steatohepatitis models, hepatic miR-205-5p levels were elevated, whereas serum levels were decreased. In HepG2 cells treated with a mixture of oleic and palmitic acids to induce fat accumulation, overexpression of miR-205-5p increased the expression of lipogenic gene (ACC) and decreased the expression of the rate-limiting enzyme for fatty acid β-oxidation (ACOX1) and transcription factors involved in fatty acid oxidation and oxidative stress (HNF4A and NRF2). Furthermore, forced expression of miR-205-5p significantly increased fat levels in HepG2 cells. These findings suggest that the PPARγ-miR-205-5p axis plays a key role in the promotion of hepatic fat accumulation. Collectively, our data indicate that miR-205-5p has potential as a downstream effector of hepatic PPARγ signaling and may serve as a biomarker and therapeutic target for nonalcoholic fatty liver disease.

Thymic T cell development shows homeostasis against various stressors. Invariant natural killer T (iNKT) cells in the thymus contribute to recovery of thymic development after irradiation owing to their initial tolerance to irradiation compared to conventional thymocytes. However, whether and how iNKT cell development recovers from irradiation remains unknown. Here we show that iNKT cells in the thymus exhibit much slower postirradiation recovery than conventional thymocytes. We observed that fluctuation of V and J genes usage does not correlate with the decrease of iNKT cell population and that irradiation markedly elevated the frequency of cell death relative to proliferation in iNKT cells. Mathematical modeling of recovery dynamics of iNKT cell progenitors implied that lack of rapid proliferation immediately after irradiation, unlike conventional thymocytes, contributes to the prolonged reduction of iNKT cell population. These findings indicate that the development of iNKT cells is subject to long-term effects of irradiation which leads to an increased rate of cell death and raise the possibility of an association between the prolonged reduction of iNKT cells after irradiation and autoimmune diseases caused by irradiation in bone marrow transplantation.

The VIIth International Workshop on SOX Transcription Factors (SOX2025) was held at the Karuizawa Prince Hotel West, Nagano, Japan, from September 8 to 11, 2025. The meeting marked the 20th anniversary of the SOX conference series and brought together 83 participants from 17 countries. Researchers presented cutting-edge studies spanning structural biology, stem cell regulation, neurodevelopment, sex determination, germ cell biology, vascular development and disease mechanisms including oncology, genetic disorders and acquired diseases. Educational and special lectures provided both historical perspectives and forward-looking visions, framing the scientific discussions in the context of developmental biology and medical science. With a rich program of oral presentations, posters, and discussions, SOX2025 strengthened the global community of SOX researchers and underscored the broad significance of these transcription factors in biology and disease.

Histone H3 lysine 9 (H3K9) methylation and heterochromatin protein 1 (HP1) are well-conserved heterochromatin epigenomes and their reader molecules. However, the details of the importance of them in heterochromatin formation still remain unclear. One reason for this is system redundancy, as multiple HP1 family proteins exist, as well as HP1 itself serving as hubs for various effector factors. To overcome these issues, we took a synthetic biology approach and introduced H3K9 methylation catalyzed by mouse H3K9 methyltransferases and HP1s into budding yeast, Saccharomyces cerevisiae (S. cerevisiae) which doesn't have this system, and examined its impact on transcription and chromatin compaction. We observed that the mammalian H3K9 methyltransferase can induce genome-wide H3K9 di- and tri-methylation in the S. cerevisiae, mainly in the gene body region, and HP1 accumulates over the H3K9 methylated regions. The forced expression of H3K9 methyltransferase and HP1 had little impact on transcription. Furthermore, Hi-C-seq analysis revealed no significant effects on the chromatin 3D structure. These results suggest that although H3K9 methylation and the recruitment of HP1 play essential roles in the epigenetic regulation of heterochromatin, they alone are not sufficient to alter the higher-order chromatin structure, at least in the gene body regions in S. cerevisiae.

Classic cadherin cell–cell adhesion molecules with self-organizing activities play roles in segregating distinct populations of cells at developing brain regions and/or boundaries. However, the protein dynamics of each cadherin subclass in the mouse embryonic brain is poorly described due to the low antigenicity. Here, we generate Cdh6-HA and Cdh8-PA tag knock-in (KI) mice by CRISPR/Cas9-mediated genome editing and establish Cdh6^HA/HA; Cdh8^PA/PA; Cdh11^EGFP/EGFP triple tag KI homo mice with normal viability and fertility. Immunostaining with specific antibodies for these tags reveals differential protein expression profiles almost comparable with mRNA in situ hybridization (ISH) results during embryonic brain development. We can additionally detect considerable levels of immunostaining signals outside the mRNA ISH-positive areas, specifically along the nerve tracts, suggesting physiological accumulation of these type II cadherin proteins along axons. By using super-resolution imaging, we further evaluate cadherin subcellular localization dynamics around the zona limitans intrathalamica to confirm that the prosomere 2/3 compartment boundary at E12.5 is maintained by the distinctive integration of Cdh6 or Cdh11 at apical attachment sites of the ventricular cells. These results highlight the value of the genetic tag KI strategy for proteins with low antigenicity and the functional relevance of type II classic cadherins in brain development.