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Sensory organ remodeling in Caenorhabditis elegans requires the zinc-finger protein ZTF-16.

Procko C, Lu Y, Shaham S - Genetics (2012)

Bottom Line: We show that ztf-16 mutants exhibit pronounced remodeling defects, which are explained, at least in part, by defects in the expression of ver-1.Expression and cell-specific rescue studies suggest that ztf-16, like ttx-1, functions within glia; however, promoter deletion studies show that ztf-16 acts through a site on the ver-1 promoter that is independent of ttx-1.Our studies identify an important component of glia remodeling and suggest that transcriptional changes may underlie glial morphological plasticity in the sensory organs of C. elegans.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Developmental Genetics, The Rockefeller University, New York, New York 10065, USA.

ABSTRACT
Neurons and glia display remarkable morphological plasticity, and remodeling of glia may facilitate neuronal shape changes. The molecular basis and control of glial shape changes is not well understood. In response to environmental stress, the nematode Caenorhabditis elegans enters an alternative developmental state, called dauer, in which glia and neurons of the amphid sensory organ remodel. Here, we describe a genetic screen aimed at identifying genes required for amphid glia remodeling. We previously demonstrated that remodeling requires the Otx-type transcription factor TTX-1 and its direct target, the receptor tyrosine kinase gene ver-1. We now find that the hunchback/Ikaros-like C2H2 zinc-finger factor ztf-16 is also required. We show that ztf-16 mutants exhibit pronounced remodeling defects, which are explained, at least in part, by defects in the expression of ver-1. Expression and cell-specific rescue studies suggest that ztf-16, like ttx-1, functions within glia; however, promoter deletion studies show that ztf-16 acts through a site on the ver-1 promoter that is independent of ttx-1. Our studies identify an important component of glia remodeling and suggest that transcriptional changes may underlie glial morphological plasticity in the sensory organs of C. elegans.

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The C2H2 zinc-finger factor ztf-16 is required for ver-1 expression. (A) A schematic of the interval on chromosome X to which mutant allele ns171 was mapped. The flanking SNPs are on cosmids F55D10 (base 14867) and C42D8 (base 5707). The regions spanned by the cosmids used for the rescue experiments shown in B are indicated, as is the position of the ztf-16 gene. (B) The number of lines carrying extrachromosomal arrays of the indicated cosmid that rescued the reduced ver-1 promoter::gfp (nsIs22) expression defect of ns171 mutant adult animals cultivated at 25°. (C) A schematic of the ztf-16 gene: exons are boxed; and regions encoding C2H2 zinc-finger domains are shaded. We isolated two splice forms of ztf-16 on the basis of EST data available from WormBase (release WS225) and have named these gene models ztf-16a and ztf-16b. The mutant ztf-16 alleles isolated in our screen are shown, and the corresponding amino acid change is indicated. Asterisks indicate a premature stop mutation.
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fig6: The C2H2 zinc-finger factor ztf-16 is required for ver-1 expression. (A) A schematic of the interval on chromosome X to which mutant allele ns171 was mapped. The flanking SNPs are on cosmids F55D10 (base 14867) and C42D8 (base 5707). The regions spanned by the cosmids used for the rescue experiments shown in B are indicated, as is the position of the ztf-16 gene. (B) The number of lines carrying extrachromosomal arrays of the indicated cosmid that rescued the reduced ver-1 promoter::gfp (nsIs22) expression defect of ns171 mutant adult animals cultivated at 25°. (C) A schematic of the ztf-16 gene: exons are boxed; and regions encoding C2H2 zinc-finger domains are shaded. We isolated two splice forms of ztf-16 on the basis of EST data available from WormBase (release WS225) and have named these gene models ztf-16a and ztf-16b. The mutant ztf-16 alleles isolated in our screen are shown, and the corresponding amino acid change is indicated. Asterisks indicate a premature stop mutation.

Mentions: To identify the gene corresponding to the ns171 complementation group, we used SNP mapping (Wicks et al. 2001) to place the ns171 mutation within an interval of ∼370 kb on chromosome X (Figure 6A). Cosmids spanning the 5′ region of this interval were injected into ns171 mutants and scored for rescue of ver-1 promoter::gfp expression in adults raised at 25°. One of these cosmids, R08E3, gave rescue (Figure 6B). Candidate coding regions were sequenced within this interval, and a single C-to-T substitution at codon 236 of the ztf-16 open reading frame was identified. This mutation is predicted to cause a premature stop (Figure 6C). ns178 mutants have the same base alteration as ns171 animals, and ns169 mutants harbor a different C-to-T mutation, at codon 131, which is also predicted to generate a premature stop (Figure 6C). Taken together, these studies demonstrate that ztf-16 is the relevant gene affected in mutants of the ns171 complementation group.


Sensory organ remodeling in Caenorhabditis elegans requires the zinc-finger protein ZTF-16.

Procko C, Lu Y, Shaham S - Genetics (2012)

The C2H2 zinc-finger factor ztf-16 is required for ver-1 expression. (A) A schematic of the interval on chromosome X to which mutant allele ns171 was mapped. The flanking SNPs are on cosmids F55D10 (base 14867) and C42D8 (base 5707). The regions spanned by the cosmids used for the rescue experiments shown in B are indicated, as is the position of the ztf-16 gene. (B) The number of lines carrying extrachromosomal arrays of the indicated cosmid that rescued the reduced ver-1 promoter::gfp (nsIs22) expression defect of ns171 mutant adult animals cultivated at 25°. (C) A schematic of the ztf-16 gene: exons are boxed; and regions encoding C2H2 zinc-finger domains are shaded. We isolated two splice forms of ztf-16 on the basis of EST data available from WormBase (release WS225) and have named these gene models ztf-16a and ztf-16b. The mutant ztf-16 alleles isolated in our screen are shown, and the corresponding amino acid change is indicated. Asterisks indicate a premature stop mutation.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3316652&req=5

fig6: The C2H2 zinc-finger factor ztf-16 is required for ver-1 expression. (A) A schematic of the interval on chromosome X to which mutant allele ns171 was mapped. The flanking SNPs are on cosmids F55D10 (base 14867) and C42D8 (base 5707). The regions spanned by the cosmids used for the rescue experiments shown in B are indicated, as is the position of the ztf-16 gene. (B) The number of lines carrying extrachromosomal arrays of the indicated cosmid that rescued the reduced ver-1 promoter::gfp (nsIs22) expression defect of ns171 mutant adult animals cultivated at 25°. (C) A schematic of the ztf-16 gene: exons are boxed; and regions encoding C2H2 zinc-finger domains are shaded. We isolated two splice forms of ztf-16 on the basis of EST data available from WormBase (release WS225) and have named these gene models ztf-16a and ztf-16b. The mutant ztf-16 alleles isolated in our screen are shown, and the corresponding amino acid change is indicated. Asterisks indicate a premature stop mutation.
Mentions: To identify the gene corresponding to the ns171 complementation group, we used SNP mapping (Wicks et al. 2001) to place the ns171 mutation within an interval of ∼370 kb on chromosome X (Figure 6A). Cosmids spanning the 5′ region of this interval were injected into ns171 mutants and scored for rescue of ver-1 promoter::gfp expression in adults raised at 25°. One of these cosmids, R08E3, gave rescue (Figure 6B). Candidate coding regions were sequenced within this interval, and a single C-to-T substitution at codon 236 of the ztf-16 open reading frame was identified. This mutation is predicted to cause a premature stop (Figure 6C). ns178 mutants have the same base alteration as ns171 animals, and ns169 mutants harbor a different C-to-T mutation, at codon 131, which is also predicted to generate a premature stop (Figure 6C). Taken together, these studies demonstrate that ztf-16 is the relevant gene affected in mutants of the ns171 complementation group.

Bottom Line: We show that ztf-16 mutants exhibit pronounced remodeling defects, which are explained, at least in part, by defects in the expression of ver-1.Expression and cell-specific rescue studies suggest that ztf-16, like ttx-1, functions within glia; however, promoter deletion studies show that ztf-16 acts through a site on the ver-1 promoter that is independent of ttx-1.Our studies identify an important component of glia remodeling and suggest that transcriptional changes may underlie glial morphological plasticity in the sensory organs of C. elegans.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Developmental Genetics, The Rockefeller University, New York, New York 10065, USA.

ABSTRACT
Neurons and glia display remarkable morphological plasticity, and remodeling of glia may facilitate neuronal shape changes. The molecular basis and control of glial shape changes is not well understood. In response to environmental stress, the nematode Caenorhabditis elegans enters an alternative developmental state, called dauer, in which glia and neurons of the amphid sensory organ remodel. Here, we describe a genetic screen aimed at identifying genes required for amphid glia remodeling. We previously demonstrated that remodeling requires the Otx-type transcription factor TTX-1 and its direct target, the receptor tyrosine kinase gene ver-1. We now find that the hunchback/Ikaros-like C2H2 zinc-finger factor ztf-16 is also required. We show that ztf-16 mutants exhibit pronounced remodeling defects, which are explained, at least in part, by defects in the expression of ver-1. Expression and cell-specific rescue studies suggest that ztf-16, like ttx-1, functions within glia; however, promoter deletion studies show that ztf-16 acts through a site on the ver-1 promoter that is independent of ttx-1. Our studies identify an important component of glia remodeling and suggest that transcriptional changes may underlie glial morphological plasticity in the sensory organs of C. elegans.

Show MeSH
Related in: MedlinePlus