The transmembrane collagen COL-99 guides longitudinally extending axons in C. elegans

Taylor, Jesse; Unsoeld, Thomas; Hutter, Harald

doi:10.1016/j.mcn.2018.03.003

Cited by 22 publications

(17 citation statements)

References 35 publications

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“…Animal studies have clarified the roles of MACITs in the peripheral nervous system. COL‐99 mutant worms display an axon pathfinding defect for ventral nerve cord motor nerves (Taylor et al, ). During worms' development, COL‐99 is expressed in the hypodermis, and in adult worms it is expressed in muscle and the NMJ, suggesting a cell non‐autonomous paradigm in axon guidance (Tu et al, ; Taylor et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…COL‐99 mutant worms display an axon pathfinding defect for ventral nerve cord motor nerves (Taylor et al, ). During worms' development, COL‐99 is expressed in the hypodermis, and in adult worms it is expressed in muscle and the NMJ, suggesting a cell non‐autonomous paradigm in axon guidance (Tu et al, ; Taylor et al, ). Interestingly, collagen XIII ectodomain support was found to enhance neurite outgrowth in cultured rat fetal hippocampal neurons (Sund et al, ).…”

Section: Introductionmentioning

confidence: 99%

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Collagen XIII and Other ECM Components in the Assembly and Disease of the Neuromuscular Junction

Heikkinen

Härönen

Norman

et al. 2019

The Anatomical Record

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Alongside playing structural roles, the extracellular matrix (ECM) acts as an interaction platform for cellular homeostasis, organ development, and maintenance. The necessity of the ECM is highlighted by the diverse, sometimes very serious diseases that stem from defects in its components. The neuromuscular junction (NMJ) is a large peripheral motor synapse differing from its central counterparts through the ECM included at the synaptic cleft. Such synaptic basal lamina (BL) is specialized to support NMJ establishment, differentiation, maturation, stabilization, and function and diverges in molecular composition from the extrasynaptic ECM. Mutations, toxins, and autoantibodies may compromise NMJ integrity and function, thereby leading to congenital myasthenic syndromes (CMSs), poisoning, and autoimmune diseases, respectively, and all these conditions may involve synaptic ECM molecules. With neurotransmission degraded or blocked, muscle function is impaired or even prevented. At worst, this can be fatal. The article reviews the synaptic BL composition required for assembly and function of the NMJ molecular machinery through the lens of studies primarily with mouse models but also with human patients. In‐depth focus is given to collagen XIII, a postsynaptic‐membrane‐spanning but also shed ECM protein that in recent years has been revealed to be a significant component for the NMJ. Its deficiency in humans causes CMS, and autoantibodies against it have been recognized in autoimmune myasthenia gravis. Mouse models have exposed numerous details that appear to recapitulate human NMJ phenotypes relatively faithfully and thereby can be readily used to generate information necessary for understanding and ultimately treating human diseases. Anat Rec, 2019. © 2019 Wiley Periodicals, Inc.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Collagen XIII and Other ECM Components in the Assembly and Disease of the Neuromuscular Junction

Heikkinen

Härönen

Norman

et al. 2019

The Anatomical Record

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“…One study revealed that the increase in collagen VI expression in the brains of hAPP mice is a neuroprotective response (Cheng et al, 2009). Other collagen genes provide guidance for axon outgrowth (Taylor et al, 2018), help motor neurons to innervate (Kowa et al, 2004), and regulate Aβ peptide formation during the progression of AD (Osada et al, 2005). Because of these important roles of collagen in neurons, we assume that the loss of collagen in the AD pineal gland is linked to pineal gland dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Analysis of Pineal Glands in the Mouse Model of Alzheimer’s Disease

Nam

Yoon

Kim

et al. 2020

Front. Mol. Neurosci.

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The pineal gland maintains the circadian rhythm in the body by secreting the hormone melatonin. Alzheimer's disease (AD) is the most common neurodegenerative disease. Pineal gland impairment in AD is widely observed, but no study to date has analyzed the transcriptome in the pineal glands of AD. To establish resources for the study on pineal gland dysfunction in AD, we performed a transcriptome analysis of the pineal glands of AD model mice and compared them to those of wild type mice. We identified the global change of diverse protein-coding RNAs, which are implicated in the alteration in cellular transport, protein transport, protein folding, collagen expression, histone dosage, and the electron transfer system. We also discovered various dysregulated long noncoding RNAs and circular RNAs in the pineal glands of mice with AD. This study showed that the expression of diverse RNAs with important functional implications in AD was changed in the pineal gland of the AD mouse model. The analyzed data reported in this study will be an important resource for future studies to elucidate the altered physiology of the pineal gland in AD.

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“…We used WGS, SNP mapping, and complementation tests to characterize the genes. hd130 is an allele of col-99, encoding a transmembrane collagen similar to the transmembrane collagen types XIII, XXIII, and XXV in vertebrates (Taylor et al 2018). Sequencing of hd130 revealed an early nonsense mutation predicted to truncate the protein after 24 amino acids ( Figure 3).…”

Section: Identification Of Mutants Leading To a Symmetrical Ventral Cordmentioning

confidence: 99%

“…A third mutation identified in the screens, hd130, is an allele of col-99, encoding a transmembrane collagen. Our recent description of the role of col-99 in axon guidance in C. elegans (Taylor et al 2018) is largely based on the allele isolated here. We have recently shown that col-99 mutants have axon guidance defects in several classes of axons in the VNC, including the command interneurons of the motor circuit.…”

Section: Genes Identified In the Genetic Screensmentioning

confidence: 99%

Multiple Pathways Act Together To Establish Asymmetry of the Ventral Nerve Cord in Caenorhabditis elegans

Taylor

Hutter

2019

Genetics

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The central nervous system of most animals is bilaterally symmetrical. Closer observation often reveals some functional or anatomical left-right asymmetries. In the nematode Caenorhabditis elegans, the most obvious asymmetry in the nervous system is found in the ventral nerve cord (VNC), where most axons are in the right axon tract. The asymmetry is established when axons entering the VNC from the brain switch from the left to the right side at the anterior end of the VNC. In genetic screens we identified several mutations compromising VNC asymmetry. This includes alleles of col-99 (encoding a transmembrane collagen), unc-52/perlecan and unc-34 (encoding the actin modulator Enabled/Vasodilator-stimulated phosphoproteins). In addition, we evaluated mutants in known axon guidance pathways for asymmetry defects and used genetic interaction studies to place the genes into genetic pathways. In total we identified four different pathways contributing to the establishment of VNC asymmetry, represented by UNC-6/netrin, SAX-3/Robo, COL-99, and EPI-1/laminin. The combined inactivation of these pathways in triple and quadruple mutants leads to highly penetrant VNC asymmetry defects, suggesting these pathways are important contributors to the establishment of VNC asymmetry in C. elegans.

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The transmembrane collagen COL-99 guides longitudinally extending axons in C. elegans

Cited by 22 publications

References 35 publications

Collagen XIII and Other ECM Components in the Assembly and Disease of the Neuromuscular Junction

Collagen XIII and Other ECM Components in the Assembly and Disease of the Neuromuscular Junction

Transcriptome Analysis of Pineal Glands in the Mouse Model of Alzheimer’s Disease

Multiple Pathways Act Together To Establish Asymmetry of the Ventral Nerve Cord in Caenorhabditis elegans

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