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Section 2: Nervous system development

Cell-type-specific promoters for C. elegans glia

ORCID Icon, ORCID Icon & ORCID Icon
Pages 335-346 | Received 28 Feb 2020, Accepted 08 Jun 2020, Published online: 22 Jul 2020
 

Abstract

Glia shape the development and function of the C. elegans nervous system, especially its sense organs and central neuropil (nerve ring). Cell-type-specific promoters allow investigators to label or manipulate individual glial cell types, and therefore provide a key tool for deciphering glial function. In this technical resource, we compare the specificity, brightness, and consistency of cell-type-specific promoters for C. elegans glia. We identify a set of promoters for the study of seven glial cell types (F16F9.3, amphid and phasmid sheath glia; F11C7.2, amphid sheath glia only; grl-2, amphid and phasmid socket glia; hlh-17, cephalic (CEP) sheath glia; and grl-18, inner labial (IL) socket glia) as well as a pan-glial promoter (mir-228). We compare these promoters to promoters that are expressed more variably in combinations of glial cell types (delm-1 and itx-1). We note that the expression of some promoters depends on external conditions or the internal state of the organism, such as developmental stage, suggesting glial plasticity. Finally, we demonstrate an approach for prospectively identifying cell-type-specific glial promoters using existing single-cell sequencing data, and we use this approach to identify two novel promoters specific to IL socket glia (col-53 and col-177).

Acknowledgements

The authors thank Shai Shaham and members of the Shaham laboratory, Meera Sundaram, and John Murray for sharing information and advice on glial-specific promoters and for providing strains and plasmids, and John Murray for help using the VisCello data explorer. The authors thank members of the Heiman laboratory for unpublished work further characterizing candidate promoters, including Ian McLachlan (itx-1), Elizabeth Cebul (grl-18, delm-1, delm-2), and Karolina Mizeracka (grl-2, lin-48). Some strains were provided by the CGC, which is funded by National Institutes of Health Office of Research Infrastructure Programs (P40 OD010440).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by NIH [T32NS007473] to L.W. and NIH [R01NS112343] to M.G.H.