scholarly journals The membrane protein Raw regulates dendrite pruning via the secretory pathway

Development ◽  
2020 ◽  
Vol 147 (19) ◽  
pp. dev191155
Author(s):  
Menglong Rui ◽  
Shufeng Bu ◽  
Liang Yuh Chew ◽  
Qiwei Wang ◽  
Fengwei Yu
Keyword(s):  
Nervous System ◽  
Cell Adhesion ◽  
Membrane Protein ◽  
Sensory Neurons ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Secretory Pathway ◽  
Molecular Mechanisms ◽  
Jnk Signaling

ABSTRACTNeuronal pruning is essential for proper wiring of the nervous systems in invertebrates and vertebrates. Drosophila ddaC sensory neurons selectively prune their larval dendrites to sculpt the nervous system during early metamorphosis. However, the molecular mechanisms underlying ddaC dendrite pruning remain elusive. Here, we identify an important and cell-autonomous role of the membrane protein Raw in dendrite pruning of ddaC neurons. Raw appears to regulate dendrite pruning via a novel mechanism, which is independent of JNK signaling. Importantly, we show that Raw promotes endocytosis and downregulation of the conserved L1-type cell-adhesion molecule Neuroglian (Nrg) prior to dendrite pruning. Moreover, Raw is required to modulate the secretory pathway by regulating the integrity of secretory organelles and efficient protein secretion. Mechanistically, Raw facilitates Nrg downregulation and dendrite pruning in part through regulation of the secretory pathway. Thus, this study reveals a JNK-independent role of Raw in regulating the secretory pathway and thereby promoting dendrite pruning.

scholarly journals Dscam1 promotes blood cell survival in Drosophila melanogaster through a dual role in blood cells and neurons

2020 ◽  
Author(s):  
Debra Ouyang ◽  
Xiaoyi Xiao ◽  
Anjeli Mase ◽  
Glenda Li ◽  
Sean Corcoran ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Sensory Neurons ◽  
Adhesion Molecule ◽  
Blood Cells ◽  
Cell Adhesion Molecule ◽  
Dual Role ◽  
Cell Adhesion Molecule 1 ◽  
Peripheral Sensory

AbstractDown Syndrome Cell Adhesion Molecule 1 (Dscam1) is a receptor-like cell adhesion molecule that is conserved across the animal kingdom, but its roles in hematopoiesis remain unknown. Dscam1 related genes in vertebrates and invertebrates are key regulators of neuron morphogenesis and neuronal tiling. In Drosophila, Dscam1 in addition has roles in blood cells (hemocytes) in innate immunity and phagocytosis of pathogens. Given the anatomical and functional role of peripheral sensory neurons as microenvironments for resident hematopoietic sites in the Drosophila larva, we sought to investigate the role of Dscam1 in this context. Interestingly, we find that Dscam1 fills the role of a previously anticipated factor in neuron-hemocyte communication that supports trophic survival: tissue specific silencing of Dscam1 by in vivo RNAi in sensory neurons leads to neuron reduction, which in turn results in reduced hemocyte numbers due to apoptosis. Dscam1 silencing in hemocytes also results in a reduction of hemocytes and increased apoptosis. This cell-autonomous effect of Dscam1 silencing can be mimicked by RNAi silencing of dreadlocks (dock), suggesting that intracellular Dscam1 signaling relies on the adapter protein Dock in this system. Our findings reveal a dual role for Dscam1 in Drosophila hematopoiesis, by promoting survival of the sensory neuron microenvironments that in turn support hemocyte survival, and by promoting survival of hemocytes cell-autonomously. It will be interesting to explore possible functions of vertebrate Dscam1 related genes such as DSCAML1 in blood cells and their trophic survival.

scholarly journals Potential role of SC1, a cell adhesion molecule, in mammary gland tumors

2008 ◽  
Author(s):  
Kenji Hagimori ◽  
Hidenori Kato ◽  
Keiko Fukuda ◽  
Masaharu Kikuta ◽  
Yasuhiro Tsukamoto ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Mammary Gland ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Potential Role ◽  
Mammary Gland Tumors ◽  
A Cell

scholarly journals The inlA Gene of Listeria monocytogenesLO28 Harbors a Nonsense Mutation Resulting in Release of Internalin

1998 ◽  
Vol 66 (7) ◽  
pp. 3420-3422 ◽  
Author(s):  
Renaud Jonquières ◽  
Hélène Bierne ◽  
Jérôme Mengaud ◽  
Pascale Cossart
Keyword(s):  
Cell Adhesion ◽  
Listeria Monocytogenes ◽  
Virulence Factor ◽  
Adhesion Molecule ◽  
Nonsense Mutation ◽  
Cell Adhesion Molecule ◽  
Culture Medium ◽  
Surface Protein ◽  
Truncated Protein

ABSTRACT Internalin is a surface protein that mediates entry ofListeria monocytogenes EGD into epithelial cells expressing the cell adhesion molecule human E-cadherin or its chicken homolog, L-CAM, which act as receptors for internalin. After observing that entry of L. monocytogenes LO28 into S180 fibroblasts, in contrast to that of EGD, did not increase after transfection with L-CAM, we examined both the expression and the structure of internalin in strain LO28. We discovered a nonsense mutation in inlA which results in a truncated protein released in the culture medium. Mutations leading to release of internalin were also detected in clinical and food isolates. These results question the role of internalin as a virulence factor in murine listeriosis.

scholarly journals The Protective Effect of Apamin on LPS/Fat-Induced Atherosclerotic Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Soo-Jung Kim ◽  
Ji-Hyun Park ◽  
Kyung-Hyun Kim ◽  
Woo-Ram Lee ◽  
Sok Cheon Pak ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Molecular Mechanisms ◽  
Atherogenic Diet ◽  
Descending Aorta ◽  
Atherosclerotic Lesions ◽  
Atherosclerotic Change ◽  
Peptide Component ◽  
Necrosis Factor

Apamin, a peptide component of bee venom (BV), has anti-inflammatory properties. However, the molecular mechanisms by which apamin prevents atherosclerosis are not fully understood. We examined the effect of apamin on atherosclerotic mice. Atherosclerotic mice received intraperitoneal (ip) injections of lipopolysaccharide (LPS, 2 mg/kg) to induce atherosclerotic change and were fed an atherogenic diet for 12 weeks. Apamin (0.05 mg/kg) was administered by ip injection. LPS-induced THP-1-derived macrophage inflammation treated with apamin reduced expression of tumor necrosis factor (TNF)-α, vascular cell adhesion molecule (VCAM)-1, and intracellular cell adhesion molecule (ICAM)-1, as well as the nuclear factor kappa B (NF-κB) signaling pathway. Apamin decreased the formation of atherosclerotic lesions as assessed by hematoxylin and elastic staining. Treatment with apamin reduced lipids, Ca2+levels, and TNF-αin the serum from atherosclerotic mice. Further, apamin significantly attenuated expression of VCAM-1, ICAM-1, TGF-β1, and fibronectin in the descending aorta from atherosclerotic mice. These results indicate that apamin plays an important role in monocyte/macrophage inflammatory processing and may be of potential value for preventing atherosclerosis.

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