The molecular signature and <i>cis</i>-regulatory architecture of a <i>C. elegans</i> gustatory neuron

Etchberger, John F.; Lorch, Adam H.; Sleumer, Monica C.; Zapf, Richard; Jones, Steven J.M.; Marra, Marco A.; Holt, Robert A.; Moerman, Donald G.; Hobert, Oliver

doi:10.1101/gad.1560107

Cited by 158 publications

(286 citation statements)

References 69 publications

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“…Taken together, die-1 expression passes through several distinct phases: an early bilateral phase, likely controlled by bilateral ASE fate determinants such as che-1 and nhr-67 (Etchberger et al 2007;Sarin et al 2009); a restriction to ASEL that requires transient activity of the cog-1 homeobox gene; and a maintenance phase that requires ceh-36 and die-1 itself to promote expression in ASEL and fozi-1 to repress expression in ASER.…”

Section: Resultsmentioning

confidence: 99%

Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

et al. 2013

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Left/right asymmetric features of animals are either randomly distributed on either the left or right side within a population (''antisymmetries'') or found stereotypically on one particular side of an animal (''directional asymmetries''). Both types of asymmetries can be found in nervous systems, but whether the regulatory programs that establish these asymmetries share any mechanistic features is not known. We describe here an unprecedented molecular link between these two types of asymmetries in Caenorhabditis elegans. The zinc finger transcription factor die-1 is expressed in a directionally asymmetric manner in the gustatory neuron pair ASE left (ASEL) and ASE right (ASER), while it is expressed in an antisymmetric manner in the olfactory neuron pair AWC left (AWCL) and AWC right (AWCR). Asymmetric die-1 expression is controlled in a fundamentally distinct manner in these two neuron pairs. Importantly, asymmetric die-1 expression controls the directionally asymmetric expression of gustatory receptor proteins in the ASE neurons and the antisymmetric expression of olfactory receptor proteins in the AWC neurons. These asymmetries serve to increase the ability of the animal to discriminate distinct chemosensory inputs.

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Section: Resultsmentioning

confidence: 99%

Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

et al. 2013

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“…(D) The ot150 mutation affects one of the invariant positions in the ASE motif, a binding site for the Znfinger transcription factor CHE-1 (Etchberger et al 2007). The ASE motif of lsy-6 binds CHE-1 in vitro (Etchberger et al 2007). CHE-1 is required to induce the hybrid precursor state in the two ASE neurons during which asymmetric regulatory and terminal differentiation factors are initially expressed in a bilaterally manner .…”

Section: Class II Mutants (2 Aser Neurons)mentioning

confidence: 99%

“…CHE-1 is required to induce the hybrid precursor state in the two ASE neurons during which asymmetric regulatory and terminal differentiation factors are initially expressed in a bilaterally manner . The ASE motif shown here is consensus build from .20 ASE expressed genes (Etchberger et al 2007). …”

Section: Class II Mutants (2 Aser Neurons)mentioning

confidence: 99%

“…Four of five lsy-6 promC Tgfp lines show expression in ASEL (12-33% penetrant; see materials and methods for comments on this transgene) and zero of four lsy-6 promC-ot150 Tgfp show expression in ASEL. (D) The ot150 mutation affects one of the invariant positions in the ASE motif, a binding site for the Znfinger transcription factor CHE-1 (Etchberger et al 2007). The ASE motif of lsy-6 binds CHE-1 in vitro (Etchberger et al 2007).…”

Section: Class II Mutants (2 Aser Neurons)mentioning

confidence: 99%

“…UNC-37, a transcriptional corepressor, likely physically interacts with COG-1 and is not shown here. che-1 is also expressed in ASEL and ASER and appears to control the expression of every gene in this regulatory network (Chang et al 2003;Etchberger et al 2007). 2005). Conceptually similar bistable systems that also utilize double-negative feedback loops composed of gene regulatory factors include the decision of phage lambda to adopt either the lytic or the lysogenic state (Ptashne 1992).…”

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Genetic Screens forCaenorhabditis elegansMutants Defective in Left/Right Asymmetric Neuronal Fate Specification

Sarin¹,

O'Meara²,

Flowers³

et al. 2007

Genetics

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We describe here the results of genetic screens for Caenorhabditis elegans mutants in which a single neuronal fate decision is inappropriately executed. In wild-type animals, the two morphologically bilaterally symmetric gustatory neurons ASE left (ASEL) and ASE right (ASER) undergo a left/right asymmetric diversification in cell fate, manifested by the differential expression of a class of putative chemoreceptors and neuropeptides. Using single cell-specific gfp reporters and screening through a total of almost 120,000 haploid genomes, we isolated 161 mutants that define at least six different classes of mutant phenotypes in which ASEL/R fate is disrupted. Each mutant phenotypic class encompasses one to nine different complementation groups. Besides many alleles of 10 previously described genes, we have identified at least 16 novel ''lsy'' genes (''laterally symmetric''). Among mutations in known genes, we retrieved four alleles of the miRNA lsy-6 and a gain-of-function mutation in the 39-UTR of a target of lsy-6, the cog-1 homeobox gene. Using newly found temperature-sensitive alleles of cog-1, we determined that a bistable feedback loop controlling ASEL vs. ASER fate, of which cog-1 is a component, is only transiently required to initiate but not to maintain ASEL and ASER fate. Taken together, our mutant screens identified a broad catalog of genes whose molecular characterization is expected to provide more insight into the complex genetic architecture of a left/right asymmetric neuronal cell fate decision.A PART from expressing a core set of features that distinguish neuronal from nonneuronal cell types, individual cell types in the nervous system express distinct batteries of genes that generate the structural and functional diversity of neuronal cell types. The diversification of cell fate in the developing nervous system presumably relies on the interplay of a host of regulatory factors. Screens for mutant animals defective in neuronal fate specification provide a powerful and unbiased approach to identify these regulatory factors. Such screens have been successfully conducted in various model systems, most prominently flies and worms, yielding valuable insights into the molecular mechanisms that control neuronal fate specification. We describe here genetic screens for neuronal fate mutants in the nematode Caenorhabditis elegans that focus on a cell fate decision executed by a single neuron class, the ASE gustatory neurons. This neuron class is composed of two morphologically bilaterally symmetric neurons, ASE We have previously reported the identification of mutants that affect the development of the left/right asymmetry of the ASE neurons (Chang et al. 2003; Hobert 2003, 2005;Johnston et al. 2006). These mutants, which we termed lsy mutants (for laterally symmetric) to indicate their role in controlling the fate of two left/right asymmetric neurons, fell into four distinct classes ( Figure 1A). In class I mutants, both ASE neurons adopt the fate of the ASEL neuron, with a concomitant loss of ASE...

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In situ hybridization of neuropeptide‐encoding transcripts afp‐1, afp‐3, and afp‐4 in neurons of the nematode ascaris suum

Nanda¹,

Stretton²

2010

J of Comparative Neurology

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The gene transcripts encoding both the AF8 and AF2 neuropeptides of the nematode Ascaris suum have been identified, cloned, and sequenced. The AF8 transcript (afp-3) encodes five identical copies of AF8; each peptide-encoding region is flanked by the appropriate dibasic or monobasic cleavage processing sites. The AF2 transcript (afp-4) encodes three identical copies of AF2 along with the appropriate cleavage sites. In contrast, the afp-1 transcript (Edison et al. [1997] Peptides 18:929 –935) encodes six different AF peptides (AF3, 4, 10, 13, 14, 20) which all share a –PGVLRFamide C-terminus but have different N-terminal sequences. By using in situ hybridization, gene transcript expression patterns of afp-1, afp-3, and afp-4 (As-flp-18, As-flp-6, and As-flp-14, respectively, in the naming convention proposed by Blaxter et al. [1997] Parasitol Today 13:416 – 417) were determined in the adult A. suum anterior nervous system. Each gene transcript can be localized to a different subset of neurons. These subsets of neurons are different from the subsets of Caenorhabditis elegans neurons that were shown to express identical or similar peptides by the use of promoter GFP constructs

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The molecular signature and cis-regulatory architecture of a C. elegans gustatory neuron

Cited by 158 publications

References 69 publications

Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

Genetic Screens forCaenorhabditis elegansMutants Defective in Left/Right Asymmetric Neuronal Fate Specification

In situ hybridization of neuropeptide‐encoding transcripts afp‐1, afp‐3, and afp‐4 in neurons of the nematode ascaris suum

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