Ono Minagi Hitomi, Sarper Safiye Esra, Kurosaka Hiroshi, Kuremoto Koh-Ichi, Taniuchi Ichiro, Sakai Takayoshi, Yamashiro Takashi
Department of Oral-facial Disorders, Osaka University Graduate School of Dentistry, Osaka, Japan.
Department of Orthodontics and Dentofacial Orthopedics, Osaka University Graduate School of Dentistry, Osaka, Japan.
PLoS One. 2017 Sep 6;12(9):e0184395. doi: 10.1371/journal.pone.0184395. eCollection 2017.
The mouse granular convoluted tubules (GCTs), which are only located in the submandibular gland (SMG) are known to develop and maintain their structure in an androgen-dependent manner. We previously demonstrated that the GCTs are involuted by the epithelial deletion of core binding factor β (CBFβ), a transcription factor that physically interacts with any of the Runt-related transcription factor (RUNX) proteins (RUNX1, 2 and 3). This result clearly demonstrates that the Runx /Cbfb signaling pathway is indispensable in the development of the GCTs. However, it is not clear which of the RUNX proteins plays useful role in the development of the GCTs by activating the Runx /Cbfb signaling pathway. Past studies have revealed that the Runx /Cbfb signaling pathway plays important roles in various aspects of development and homeostatic events. Moreover, the Runx genes have different temporospatial requirements depending on the biological situation. In the present study, the GCTs of the SMG showed a remarkable phenotype of, which phenocopied the epithelial deletion of Cbfb, in epithelial-specific Runx1 conditional knock-out (cKO) mice. The results indicate that Runx1 works as a partner of Cbfb during the development of the GCTs. We also discovered that the depletion of Runx1 resulted in the reduced secretion of saliva in male mice. Consistent with this finding, one of the water channels, Aquaporin-5 (AQP5) was mislocalized in the cytoplasm of the Runx1 mutants, suggesting a novel role of Runx1 in the membrane trafficking of AQP5. In summary, the present findings demonstrated that RUNX1 is essential for the development of the GCTs. Furthermore, RUNX1 could also be involved in the membrane trafficking of the AQP5 protein of the acinar cells in the SMG in order to allow for the proper secretion of saliva.
小鼠颗粒曲管(GCTs)仅位于下颌下腺(SMG),已知其以雄激素依赖的方式发育并维持其结构。我们先前证明,核心结合因子β(CBFβ)的上皮缺失会导致GCTs退化,CBFβ是一种转录因子,可与任何Runt相关转录因子(RUNX)蛋白(RUNX1、2和3)发生物理相互作用。这一结果清楚地表明,Runx/Cbfb信号通路在GCTs的发育中不可或缺。然而,尚不清楚哪种RUNX蛋白通过激活Runx/Cbfb信号通路在GCTs的发育中发挥作用。过去的研究表明,Runx/Cbfb信号通路在发育和稳态事件的各个方面都发挥着重要作用。此外,Runx基因根据生物学情况具有不同的时空需求。在本研究中,在上皮特异性Runx1条件性敲除(cKO)小鼠中,SMG的GCTs表现出一种显著的表型,该表型模仿了Cbfb的上皮缺失。结果表明,Runx1在GCTs发育过程中作为Cbfb的伙伴发挥作用。我们还发现,Runx1的缺失导致雄性小鼠唾液分泌减少。与此发现一致的是,水通道蛋白5(AQP5)这一水通道之一在Runx1突变体的细胞质中定位错误,这表明Runx1在AQP5的膜转运中具有新作用。总之,本研究结果表明RUNX1对GCTs的发育至关重要。此外,RUNX1还可能参与SMG腺泡细胞AQP5蛋白的膜转运,以实现唾液的正常分泌。