ALS2 regulates endosomal trafficking, postsynaptic development, and neuronal survival

Mutations in the human ALS2 gene cause recessive juvenile-onset amyotrophic lateral sclerosis and related motor neuron diseases. Although the ALS2 protein has been identified as a guanine-nucleotide exchange factor for the small GTPase Rab5, its physiological roles remain largely unknown. Here, we d...

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Veröffentlicht in:The Journal of cell biology 2021-05, Vol.220 (5), p.1
Hauptverfasser: Kim, Joohyung, Kim, Sungdae, Nahm, Minyeop, Li, Tsai-Ning, Lin, Hsin-Chieh, Kim, Yeongjin David, Lee, Jihye, Yao, Chi-Kuang, Lee, Seungbok
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container_title The Journal of cell biology
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creator Kim, Joohyung
Kim, Sungdae
Nahm, Minyeop
Li, Tsai-Ning
Lin, Hsin-Chieh
Kim, Yeongjin David
Lee, Jihye
Yao, Chi-Kuang
Lee, Seungbok
description Mutations in the human ALS2 gene cause recessive juvenile-onset amyotrophic lateral sclerosis and related motor neuron diseases. Although the ALS2 protein has been identified as a guanine-nucleotide exchange factor for the small GTPase Rab5, its physiological roles remain largely unknown. Here, we demonstrate that the Drosophila homologue of ALS2 (dALS2) promotes postsynaptic development by activating the Frizzled nuclear import (FNI) pathway. dALS2 loss causes structural defects in the postsynaptic subsynaptic reticulum (SSR), recapitulating the phenotypes observed in FNI pathway mutants. Consistently, these developmental phenotypes are rescued by postsynaptic expression of the signaling-competent C-terminal fragment of Drosophila Frizzled-2 (dFz2). We further demonstrate that dALS2 directs early to late endosome trafficking and that the dFz2 C terminus is cleaved in late endosomes. Finally, dALS2 loss causes age-dependent progressive defects resembling ALS, including locomotor impairment and brain neurodegeneration, independently of the FNI pathway. These findings establish novel regulatory roles for dALS2 in endosomal trafficking, synaptic development, and neuronal survival.
doi_str_mv 10.1083/jcb.202007112
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Although the ALS2 protein has been identified as a guanine-nucleotide exchange factor for the small GTPase Rab5, its physiological roles remain largely unknown. Here, we demonstrate that the Drosophila homologue of ALS2 (dALS2) promotes postsynaptic development by activating the Frizzled nuclear import (FNI) pathway. dALS2 loss causes structural defects in the postsynaptic subsynaptic reticulum (SSR), recapitulating the phenotypes observed in FNI pathway mutants. Consistently, these developmental phenotypes are rescued by postsynaptic expression of the signaling-competent C-terminal fragment of Drosophila Frizzled-2 (dFz2). We further demonstrate that dALS2 directs early to late endosome trafficking and that the dFz2 C terminus is cleaved in late endosomes. Finally, dALS2 loss causes age-dependent progressive defects resembling ALS, including locomotor impairment and brain neurodegeneration, independently of the FNI pathway. 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Kim, Sungdae ; Nahm, Minyeop ; Li, Tsai-Ning ; Lin, Hsin-Chieh ; Kim, Yeongjin David ; Lee, Jihye ; Yao, Chi-Kuang ; Lee, Seungbok</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-67b6cb140104bbbc0c8d70d236db87d048c1a8b614ba031b9a11769480f93eb13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Age</topic><topic>Amyotrophic lateral sclerosis</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Amyotrophic Lateral Sclerosis - metabolism</topic><topic>Animals</topic><topic>Biological Transport - physiology</topic><topic>C-Terminus</topic><topic>Cell Death - genetics</topic><topic>Cell Survival - genetics</topic><topic>Cells, Cultured</topic><topic>Defects</topic><topic>Disease Models, Animal</topic><topic>Drosophila</topic><topic>Drosophila - genetics</topic><topic>Drosophila - metabolism</topic><topic>Drosophila - physiology</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Endosomes</topic><topic>Endosomes - genetics</topic><topic>Endosomes - metabolism</topic><topic>Endosomes - physiology</topic><topic>Frizzled protein</topic><topic>Fruit flies</topic><topic>GTP-binding protein</topic><topic>Guanine</topic><topic>Guanine Nucleotide Exchange Factors - genetics</topic><topic>Guanine Nucleotide Exchange Factors - metabolism</topic><topic>Homology</topic><topic>Insects</topic><topic>Juveniles</topic><topic>Motor neuron diseases</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neurodegeneration</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Neuroscience</topic><topic>Nuclear transport</topic><topic>Nucleotides</topic><topic>Phenotype</topic><topic>Phenotypes</topic><topic>Physiological effects</topic><topic>Post-Synaptic Density - genetics</topic><topic>Post-Synaptic Density - metabolism</topic><topic>Post-Synaptic Density - physiology</topic><topic>Protein transport</topic><topic>rab5 GTP-Binding Proteins - genetics</topic><topic>rab5 GTP-Binding Proteins - metabolism</topic><topic>Rab5 protein</topic><topic>Survival</topic><topic>Synaptogenesis</topic><topic>Trafficking</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Joohyung</creatorcontrib><creatorcontrib>Kim, Sungdae</creatorcontrib><creatorcontrib>Nahm, Minyeop</creatorcontrib><creatorcontrib>Li, Tsai-Ning</creatorcontrib><creatorcontrib>Lin, Hsin-Chieh</creatorcontrib><creatorcontrib>Kim, Yeongjin David</creatorcontrib><creatorcontrib>Lee, Jihye</creatorcontrib><creatorcontrib>Yao, Chi-Kuang</creatorcontrib><creatorcontrib>Lee, Seungbok</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; 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subjects Age
Amyotrophic lateral sclerosis
Amyotrophic Lateral Sclerosis - genetics
Amyotrophic Lateral Sclerosis - metabolism
Animals
Biological Transport - physiology
C-Terminus
Cell Death - genetics
Cell Survival - genetics
Cells, Cultured
Defects
Disease Models, Animal
Drosophila
Drosophila - genetics
Drosophila - metabolism
Drosophila - physiology
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
Endosomes
Endosomes - genetics
Endosomes - metabolism
Endosomes - physiology
Frizzled protein
Fruit flies
GTP-binding protein
Guanine
Guanine Nucleotide Exchange Factors - genetics
Guanine Nucleotide Exchange Factors - metabolism
Homology
Insects
Juveniles
Motor neuron diseases
Mutation
Mutation - genetics
Neurodegeneration
Neurons - metabolism
Neurons - physiology
Neuroscience
Nuclear transport
Nucleotides
Phenotype
Phenotypes
Physiological effects
Post-Synaptic Density - genetics
Post-Synaptic Density - metabolism
Post-Synaptic Density - physiology
Protein transport
rab5 GTP-Binding Proteins - genetics
rab5 GTP-Binding Proteins - metabolism
Rab5 protein
Survival
Synaptogenesis
Trafficking
title ALS2 regulates endosomal trafficking, postsynaptic development, and neuronal survival
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