Top: Inhibition of mTOR signaling rescues cilia formation in Wnt activated cells. RPE1 cells stably expressing mCherry-GFP-LC3 were treated with Co-CM and Wnt3a-CM and fixed 16 h after serum starvation for direct fluorescence analysis of mCherry and GFP signals. Representative images show GFP+mCherry+ foci (yellow dots, autophagosomes). Bottom: Model of how Wnt signaling affects ciliogenesis. Basal Wnt signaling promotes cilia formation, whereas Wnt hyperactivation prior to ciliogenesis delays this process by increasing mTORC1 activity and impairing the removal of OFD1 from centriolar satellites. M, mother centriole; D, daughter centriole.

The #PrimaryCilium regulates several signaling pathways, but what role do these pathways play in #cilium formation? This study shows that modulating Wnt & mTOR signaling affects #ciliogenesis in human retinal epithelial cells @plosbiology.org 🧪 plos.io/45Yg5gB

Top: Inhibition of mTOR signaling rescues cilia formation in Wnt activated cells. RPE1 cells stably expressing mCherry-GFP-LC3 were treated with Co-CM and Wnt3a-CM and fixed 16 h after serum starvation for direct fluorescence analysis of mCherry and GFP signals. Representative images show GFP+mCherry+ foci (yellow dots, autophagosomes). Bottom: Model of how Wnt signaling affects ciliogenesis. Basal Wnt signaling promotes cilia formation, whereas Wnt hyperactivation prior to ciliogenesis delays this process by increasing mTORC1 activity and impairing the removal of OFD1 from centriolar satellites. M, mother centriole; D, daughter centriole.

The #PrimaryCilium regulates several signaling pathways, but what role do these pathways play in #cilium formation? This study shows that modulating Wnt & mTOR signaling affects #ciliogenesis in human retinal epithelial cells @plosbiology.org 🧪 plos.io/45Yg5gB

Top: Inhibition of mTOR signaling rescues cilia formation in Wnt activated cells. RPE1 cells stably expressing mCherry-GFP-LC3 were treated with Co-CM and Wnt3a-CM and fixed 16 h after serum starvation for direct fluorescence analysis of mCherry and GFP signals. Representative images show GFP+mCherry+ foci (yellow dots, autophagosomes). Bottom: Model of how Wnt signaling affects ciliogenesis. Basal Wnt signaling promotes cilia formation, whereas Wnt hyperactivation prior to ciliogenesis delays this process by increasing mTORC1 activity and impairing the removal of OFD1 from centriolar satellites. M, mother centriole; D, daughter centriole.

The #PrimaryCilium regulates several signaling pathways, but what role do these pathways play in #cilium formation? This study shows that modulating Wnt & mTOR signaling affects #ciliogenesis in human retinal epithelial cells @plosbiology.org 🧪 plos.io/45Yg5gB

Model for cellular functions and mechanisms of CCDC66. CCDC66 is a microtubule-stabilizing protein that maintains cilium integrity and size and facilitates vesicular transport at the ciliary base. Depletion of CCDC66 results in variations in cilia size due to compromised axonemal integrity, intraflagellar transport, and increased ectocytosis events involving the release of vesicles and fragments. CCDC66 may also support ciliary ectocytosis and length stability by regulating the actin cytoskeleton. Furthermore, disruptions in both microtubule stability and the actin cytoskeleton impair RAB11 and RAB5-mediated endocytosis and membrane recycling, affecting cell adhesion and the targeting of ciliary receptors. This disruption subsequently activates protein degradation pathways through RAB7-regulated late endocytosis, potentially involving RAB7 translocation to cilia to support ectocytosis. Collectively, these defects in protein transport, cilia function, and cell contacts contribute to compromised epithelial tissue integrity and multilumen formation in kidney tubules.

The #PrimaryCilium dynamically assembles & disassembles, but how is this controlled? @cytolabkoc.bsky.social shows that #ciliopathy linked protein Ccdc66 regulates both #cilium stability & length in epithelial cells via microtubules, actin & vesicular trafficking @plosbiology.org 🧪 plos.io/4mdTS4A

Model for cellular functions and mechanisms of CCDC66. CCDC66 is a microtubule-stabilizing protein that maintains cilium integrity and size and facilitates vesicular transport at the ciliary base. Depletion of CCDC66 results in variations in cilia size due to compromised axonemal integrity, intraflagellar transport, and increased ectocytosis events involving the release of vesicles and fragments. CCDC66 may also support ciliary ectocytosis and length stability by regulating the actin cytoskeleton. Furthermore, disruptions in both microtubule stability and the actin cytoskeleton impair RAB11 and RAB5-mediated endocytosis and membrane recycling, affecting cell adhesion and the targeting of ciliary receptors. This disruption subsequently activates protein degradation pathways through RAB7-regulated late endocytosis, potentially involving RAB7 translocation to cilia to support ectocytosis. Collectively, these defects in protein transport, cilia function, and cell contacts contribute to compromised epithelial tissue integrity and multilumen formation in kidney tubules.

The #PrimaryCilium dynamically assembles & disassembles, but how is this controlled? @cytolabkoc.bsky.social shows that #ciliopathy linked protein Ccdc66 regulates both #cilium stability & length in epithelial cells via microtubules, actin & vesicular trafficking @plosbiology.org 🧪 plos.io/4mdTS4A

Model for cellular functions and mechanisms of CCDC66. CCDC66 is a microtubule-stabilizing protein that maintains cilium integrity and size and facilitates vesicular transport at the ciliary base. Depletion of CCDC66 results in variations in cilia size due to compromised axonemal integrity, intraflagellar transport, and increased ectocytosis events involving the release of vesicles and fragments. CCDC66 may also support ciliary ectocytosis and length stability by regulating the actin cytoskeleton. Furthermore, disruptions in both microtubule stability and the actin cytoskeleton impair RAB11 and RAB5-mediated endocytosis and membrane recycling, affecting cell adhesion and the targeting of ciliary receptors. This disruption subsequently activates protein degradation pathways through RAB7-regulated late endocytosis, potentially involving RAB7 translocation to cilia to support ectocytosis. Collectively, these defects in protein transport, cilia function, and cell contacts contribute to compromised epithelial tissue integrity and multilumen formation in kidney tubules.

The #PrimaryCilium dynamically assembles & disassembles, but how is this controlled? @cytolabkoc.bsky.social shows that #ciliopathy linked protein Ccdc66 regulates both #cilium stability & length in epithelial cells via microtubules, actin & vesicular trafficking @plosbiology.org 🧪 plos.io/4mdTS4A

Here we show how #microglia contact #pericytes and #endothelialcells in the #venule end of the #capillary bed. Note also how a #primarycilium of an #interneuron invaginates the microglia. But why? 🤔 journals.sagepub.com/doi/full/10.... @gazz4science.bsky.social