LMTK1 regulates dendritic formation by regulating movement of Rab11A-positive endosomes

Takano, Tetsuya; Urushibara, Tomoki; Yoshioka, Nozomu; Saito, Taro; Fukuda, Mitsunori; Tomomura, Mineko; Hisanaga, Shin Ichi

doi:10.1091/mbc.e14-01-0675

Cited by 30 publications

(48 citation statements)

References 46 publications

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“…This fits with the finding that the Rab11-binding N-terminus of Protrudin is required for its function and the notion that endocytic recycling is important for neurite outgrowth [31]. However, it is the active, GTP-bound form of Rab11 that promotes endocytic recycling and neurite outgrowth, and depletion of Rab11 has been found to prevent neurite outgrowth [30,[32][33][34]. The interaction of Protrudin with Rab11-GDP is therefore unlikely to promote recycling directly and might instead be a mechanism to attenuate Rab11 function in the growing neurite.…”

Section: Er-le Contact Site-mediated Endosome Positioning In Protrusisupporting

confidence: 84%

ER–endosome contact sites in endosome positioning and protrusion outgrowth

Raiborg

Wenzel

Pedersen

et al. 2016

Biochemical Society Transactions

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The endoplasmic reticulum (ER) makes abundant contacts with endosomes, and the numbers of contact sites increase as endosomes mature. It is already clear that such contact sites have diverse compositions and functions, but in this mini-review we will focus on two particular types of ER-endosome contact sites that regulate endosome positioning. Formation of ER-endosome contact sites that contain the cholesterol-binding protein oxysterol-binding protein-related protein 1L (ORP1L) is coordinated with loss of the minus-end-directed microtubule motor Dynein from endosomes. Conversely, formation of ER-endosome contact sites that contain the Kinesin-1-binding protein Protrudin results in transfer of the plus-end-directed microtubule motor Kinesin-1 from ER to endosomes. We discuss the possibility that formation of these two types of contact sites is coordinated as a 'gear-shift' mechanism for endosome motility, and we review evidence that Kinesin-1-mediated motility of late endosomes (LEs) to the cell periphery promotes outgrowth of neurites and other protrusions.

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Section: Er-le Contact Site-mediated Endosome Positioning In Protrusisupporting

confidence: 84%

ER–endosome contact sites in endosome positioning and protrusion outgrowth

Raiborg

Wenzel

Pedersen

et al. 2016

Biochemical Society Transactions

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“…HSP105 (Gene ID 15505) is a major heat shock protein, and it can protect against stress-induced apoptosis (36) and reduce the aggregation of denatured proteins and cytotoxicity (37). LMTK1 (Gene ID 9625) regulates neuronal cell differentiation (38,39) and is also selected in the AS. Because the AS stresses are characterized by high UV, high temperature, and drought, these genes were positively selected to adapt spiny mice of the AS to its slopespecific stresses.…”

Section: Resultsmentioning

confidence: 99%

Sympatric speciation of spiny mice, Acomys , unfolded transcriptomically at Evolution Canyon, Israel

Wang

Cai

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Spiny mice, Acomys cahirinus, colonized Israel 30,000 y ago from dry tropical Africa and inhabited rocky habitats across Israel. Earlier, we had shown by mtDNA that A. cahirinus incipiently sympatrically speciates at Evolution Canyon I (EC I) in Mount Carmel, Israel because of microclimatic interslope divergence. The EC I microsite consists of a dry and hot savannoid "African" slope (AS) and an abutting humid and cool-forested "European" slope (ES). Here, we substantiate incipient SS in A. cahirinus at EC I based on the entire transcriptome, showing that multiple slope-specific adaptive complexes across the transcriptome result in two divergent clusters. Tajima's D distribution of the abutting Acomys interslope populations shows that the ES population is under stronger positive selection, whereas the AS population is under balancing selection, harboring higher genetic polymorphisms. Considerable sites of the two populations were differentiated with a coefficient of F ST = 0.25-0.75. Remarkably, 24 and 37 putatively adaptively selected genes were detected in the AS and ES populations, respectively. The AS genes involved DNA repair, growth arrest, neural cell differentiation, and heat-shock proteins adapting to the local AS stresses of high solar radiation, drought, and high temperature. In contrast, the ES genes involved high ATP associated with energetics stress. The sharp ecological interslope divergence led to strong slope-specific selection overruling the interslope gene flow. Earlier tests suggested slope-specific mate choice. Habitat interslope-adaptive selection across the transcriptome and mate choice substantiate sympatric speciation (SS), suggesting its prevalence at EC I and commonality in nature.adaptive ecological speciation | microclimate | natural selection | RNA-seq

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“…For example, miR-338 is encoded intronically within its host gene, the apoptosis-associated tyrosine kinase ( AATK ), a gene implicated in neuroblastoma differentiation and the control of axon and dendrite outgrowth in cortical neurons [23–25]. In addition, miR-338 is enriched in the axons of sympathetic neurons [26] and is capable of locally modulating mitochondrial activity by regulating cytochrome c oxidase, subunit IV (COXIV) in the distal parts of axons [27].…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-338 Attenuates Cortical Neuronal Outgrowth by Modulating the Expression of Axon Guidance Genes

et al. 2016

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MicroRNAs (miRs) are small non-coding RNAs that confer robustness to gene networks through post-transcriptional gene regulation. Previously, we identified miR-338 as a modulator of axonal outgrowth in sympathetic neurons. In the current study, we examined the role of miR-338 in the development of cortical neurons and uncovered its downstream mRNA targets. Long-term inhibition of miR-338 during neuronal differentiation resulted in reduced dendritic complexity and altered dendritic spine morphology. Furthermore, monitoring axon outgrowth in cortical cells revealed that miR-338 overexpression decreased, whereas inhibition of miR-338 increased axonal length. To identify gene targets mediating the observed phenotype, we inhibited miR-338 in cortical neurons and performed whole-transcriptome analysis. Pathway analysis revealed that miR-338 modulates a subset of transcripts involved in the axonal guidance machinery by means of direct and indirect gene targeting. Collectively, our results implicate miR-338 as a novel regulator of cortical neuronal maturation by fine-tuning the expression of gene networks governing cortical outgrowth.

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LMTK1 regulates dendritic formation by regulating movement of Rab11A-positive endosomes

Cited by 30 publications

References 46 publications

ER–endosome contact sites in endosome positioning and protrusion outgrowth

ER–endosome contact sites in endosome positioning and protrusion outgrowth

Sympatric speciation of spiny mice, Acomys , unfolded transcriptomically at Evolution Canyon, Israel

MicroRNA-338 Attenuates Cortical Neuronal Outgrowth by Modulating the Expression of Axon Guidance Genes

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