Dye-filling of the amphid sheath glia: Implications for the functional relationship between sensory neurons and glia in Caenorhabditis elegans

Ohkura, Kiyotaka; Bürglin, Thomas R.

doi:10.1016/j.bbrc.2011.02.003

Cited by 12 publications

(8 citation statements)

References 28 publications

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“…Similar observations have been made in animals expressing GFP-tagged glia-secreted proteins (Ohkura and Burglin 2011). A microarray analysis of AMsh glia identified 298 genes whose expression is glia enriched.…”

Section: Glia and Sensory Plasticitysupporting

confidence: 59%

“…Most of the secretory apparatus in these glia is located adjacent to the amphid sensory compartment (Ward et al 1975;Perkins et al 1986), and at least some glia-enriched proteins are secreted into the extracellular space surrounding sensory receptive endings (Perens and Shaham 2005;Ohkura and Burglin 2011). These observations suggest the interesting possibility that neurons report on their activity to glia, which respond by secreting factors that adjust neuronal activity.…”

Section: Glia In C Elegans Nervous Systemmentioning

confidence: 80%

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Glial Development and Function in the Nervous System ofCaenorhabditis elegans

Shaham

2015

Cold Spring Harb Perspect Biol

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The nematode, Caenorhabditis elegans, has served as a fruitful setting for understanding conserved biological processes. The past decade has seen the rise of this model organism as an important tool for uncovering the mysteries of the glial cell, which partners with neurons to generate a functioning nervous system in all animals. C. elegans affords unparalleled single-cell resolution in vivo in examining glia -neuron interactions, and similarities between C. elegans and vertebrate glia suggest that lessons learned from this nematode are likely to have general implications. Here, I summarize what has been gleaned over the past decade since C. elegans glia research became a concerted area of focus. Studies have revealed that glia are essential elements of a functioning C. elegans nervous system and play key roles in its development. Importantly, glial influence on neuronal function appears to be dynamic. Key questions for the field to address in the near-and long-term have emerged, and these are discussed within. Single-celled and invertebrate organisms are key settings for understanding basic biology. The molecular clockworks underlying common processes, such as the cell cycle, cell death, innate immunity, RNA interference, developmental patterning, cell polarity establishment, vesicular secretion, and neuronal guidance, to name but a few, were all initially described in such model systems. Contributing to this roaring success are two properties of such systems: ease of use, and exaggeration of the phenomena under study. Caenorhabditis elegans, with its facile genetics (Brenner 1974) and small cell number (959 somatic cells in the adult hermaphrodite) (Sulston and Horvitz 1977;Sulston et al. 1983), has allowed the investigation of animal development and cell -cell interactions in vivo with unprecedented single-cell resolution. It is, therefore, an exciting choice for a model system to investigate the basic properties of glia and their interactions with neurons during nervous system development and function.The studies described in this review reveal similarities between glia in C. elegans and other animals in morphology, development, anatomy, and function, and describe new paradigms that may be broadly conserved. Differences between glia in C. elegans and in other organisms are also apparent. For example, C. elegans axons are not myelinated (White et al. 1986), probably because axon lengths are short (,1 mm). One difference, however, is of tremendous experimental utility. Unlike neurons in other model systems, C. elegans neurons can survive in vivo

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Section: Glia and Sensory Plasticitysupporting

confidence: 59%

Section: Glia In C Elegans Nervous Systemmentioning

confidence: 80%

Glial Development and Function in the Nervous System ofCaenorhabditis elegans

Shaham

2015

Cold Spring Harb Perspect Biol

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“…Since DTR was expressed only in SGNs (not in Schwann cells), we believe that the damage to Schwann cells and demyelination were secondary to SGN damage. This is supported by the fact that the intact morphology and functions of glia cells depends on the health of the neurons they cover 26, 27 . Since the surviving nerve fibers showed irregular shape and reduced diameters in the Cre + group (Fig.…”

Section: Discussionmentioning

confidence: 99%

Auditory Neuropathy after Damage to Cochlear Spiral Ganglion Neurons in Mice Resulting from Conditional Expression of Diphtheria Toxin Receptors

Pan

Song

Wang

et al. 2017

Sci Rep

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Auditory neuropathy (AN) is a hearing disorder characterized by normal cochlear amplification to sound but poor temporal processing and auditory perception in noisy backgrounds. These deficits likely result from impairments in auditory neural synchrony; such dyssynchrony of the neural responses has been linked to demyelination of auditory nerve fibers. However, no appropriate animal models are currently available that mimic this pathology. In this study, Cre-inducible diphtheria toxin receptor (iDTR +/+) mice were cross-mated with mice containing Cre (Bhlhb5-Cre +/−) specific to spiral ganglion neurons (SGNs). In double-positive offspring mice, the injection of diphtheria toxin (DT) led to a 30–40% rate of death for SGNs, but no hair cell damage. Demyelination types of pathologies were observed around the surviving SGNs and their fibers, many of which were distorted in shape. Correspondingly, a significant reduction in response synchrony to amplitude modulation was observed in this group of animals compared to the controls, which had a Cre− genotype. Taken together, our results suggest that SGN damage following the injection of DT in mice with Bhlhb5-Cre +/− and iDTR +/− is likely to be a good AN model of demyelination.

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“…They have ciliated endings at the tip of the dendrites that are open to the environment (White et al, 1986;Wood, 1988), and function as chemosensory cells that negatively modulate reversals to repellents (Hilliard et al, 2002). A simple test, dye-filling, can show if amphid and phasmid neurons are open towards the environment and are able to take up dye through their dendritic endings (Hedgecock et al, 1985;Ohkura and Bürglin, 2011;Perkins et al, 1986;Tong and Bürglin, 2010). The fluorescent dye DiI can stain strongly the sensory neurons ASH, ASJ, ASK, ADL (and weakly AWB, ASI) in the head, and PHA, PHB in the tail.…”

Section: Phasmid Dye-filling Defects In Ceh-14 Mutantsmentioning

confidence: 99%

The LIM homeobox gene ceh-14 is required for phasmid function and neurite outgrowth

Kagoshima¹,

Cassata²,

Tong³

et al. 2013

Developmental Biology

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Transcription factors play key roles in cell fate specification and cell differentiation. Previously, we showed that the LIM homeodomain factor CEH-14 is expressed in the AFD neurons where it is required for thermotaxis behavior in Caenorhabditis elegans. Here, we show that ceh-14 is expressed in the phasmid sensory neurons, PHA and PHB, a number of neurons in the tail, i.e., PHC, DVC, PVC, PVN, PVQ, PVT, PVW and PVR, as well as the touch neurons. Analysis of the promoter region shows that important regulatory elements for the expression in most neurons reside from -4kb to -1.65kb upstream of the start codon. Further, within the first introns are elements for expression in the hypodermis. Phylogenetic footprinting revealed numerous conserved motifs in these regions. In addition to the existing deletion mutation ceh-14(ch3), we isolated a new allele, ceh-14(ch2), in which only one LIM domain is disrupted. The latter mutant allele is partially defective for thermosensation. Analysis of both mutant alleles showed that they are defective in phasmid dye-filling. However, the cell body, dendritic outgrowth and ciliated endings of PHA and PHB appear normal, indicating that ceh-14 is not required for growth. The loss of a LIM domain in the ceh-14(ch2) allele causes a partial loss-of-function phenotype. Examination of the neurites of ALA and tail neurons using a ceh-14::GFP reporter shows abnormal axonal outgrowth and pathfinding.

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Dye-filling of the amphid sheath glia: Implications for the functional relationship between sensory neurons and glia in Caenorhabditis elegans

Cited by 12 publications

References 28 publications

Glial Development and Function in the Nervous System ofCaenorhabditis elegans

Glial Development and Function in the Nervous System ofCaenorhabditis elegans

Auditory Neuropathy after Damage to Cochlear Spiral Ganglion Neurons in Mice Resulting from Conditional Expression of Diphtheria Toxin Receptors

The LIM homeobox gene ceh-14 is required for phasmid function and neurite outgrowth

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