Control of neuronal subtype identity by the <i>C. elegans</i> ARID protein CFI-1

Shaham, Shai; Bargmann, Cornelia I.

doi:10.1101/gad.976002

Cited by 45 publications

(80 citation statements)

References 55 publications

(62 reference statements)

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“…To determine whether the region of R09F10 identified was part of a protein-coding gene, we inspected the genomic sequence manually and assembled a putative gene structure. Using the polymerase chain reaction (PCR) and primers corresponding to the predicted gene, we were able to amplify a cDNA from a mixed-stage cDNA library we constructed 34 (S Shaham, unpublished data). The existence of a cDNA suggested that the region of R09F10 we identified indeed contained a transcribed gene, designated R09F10.9.…”

Section: Ced-13 Encodes a Conserved Bh3-only Proteinmentioning

confidence: 99%

C. elegans ced-13 can promote apoptosis and is induced in response to DNA damage

et al. 2004

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The p53 tumor suppressor promotes apoptosis in response to DNA damage. Here we describe the Caenorhabditis elegans gene ced-13, which encodes a conserved BH3-only protein.We show that ced-13 mRNA accumulates following DNA damage, and that this accumulation is dependent on an intact C. elegans cep-1/p53 gene. We demonstrate that CED-13 protein physically interacts with the antiapoptotic Bcl-2-related protein CED-9. Furthermore, overexpression of ced-13 in somatic cells leads to the death of cells that normally survive, and this death requires the core apoptotic pathway of C. elegans. Recent studies have implicated two BH3-only proteins, Noxa and PUMA, in p53-induced apoptosis in mammals. Our studies suggest that in addition to the BH3-only protein EGL-1, CED-13 might also promote apoptosis in the C. elegans germ line in response to p53 activation. We propose that an evolutionarily conserved pathway exists in which p53 promotes cell death by inducing expression of two BH3-only genes.

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Section: Ced-13 Encodes a Conserved Bh3-only Proteinmentioning

confidence: 99%

C. elegans ced-13 can promote apoptosis and is induced in response to DNA damage

et al. 2004

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“…We also observed almost complete loss of GFP expression at the CEM positions in several other unc-86 loss-of-function mutants (Table 3). UNC-86 is expressed in 47 neurons during C. elegans development, including male CEMs and hermaphrodite HSNs (Finney and Ruvkun 1990), and is critical for the proper differentiation of these UNC-86-expressing neurons, including the differentiation and survival of CEM neurons in males (Finney et al 1988;Shaham and Bargmann 2002). Interestingly, the mouse ortholog of UNC-86, Brn3c, has been shown to act genetically upstream of the mouse BarH homeodomain protein Barhl1 to promote terminal differentiation and survival of mechanosensory hair cells (Li et al 2002), suggesting a conserved regulatory relationship between these two types of homeodomain proteins.…”

Section: Unc-86 Is Required For Cem Cell Fate Specification Independementioning

confidence: 99%

Control of sex-specific apoptosis in C. elegans by the BarH homeodomain protein CEH-30 and the transcriptional repressor UNC-37/Groucho

Peden¹,

Kimberly²,

Gengyo-Ando³

et al. 2007

Genes Dev.

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Apoptosis is essential for proper development and tissue homeostasis in metazoans. It plays a critical role in generating sexual dimorphism by eliminating structures that are not needed in a specific sex. The molecular mechanisms that regulate sexually dimorphic apoptosis are poorly understood. Here we report the identification of the ceh-30 gene as a key regulator of sex-specific apoptosis in Caenorhabditis elegans. Loss-of-function mutations in ceh-30 cause the ectopic death of male-specific CEM neurons. ceh-30 encodes a BarH homeodomain protein that acts downstream from the terminal sex determination gene tra-1, but upstream of, or in parallel to, the cell-death-initiating gene egl-1 to protect CEM neurons from undergoing apoptosis in males. The second intron of the ceh-30 gene contains two adjacent cis-elements that are binding sites for TRA-1A and a POU-type homeodomain protein UNC-86 and acts as a sensor to regulate proper specification of the CEM cell fate. Surprisingly, the N terminus of CEH-30 but not its homeodomain is critical for CEH-30's cell death inhibitory activity in CEMs and contains a conserved eh1/FIL domain that is important for the recruitment of the general transcriptional repressor UNC-37/Groucho. Our study suggests that ceh-30 defines a critical checkpoint that integrates the sex determination signal TRA-1 and the cell fate determination and survival signal UNC-86 to control the sex-specific activation of the cell death program in CEMs through the general transcription repressor UNC-37.[Keywords: C. elegans; apoptosis; sex-specific; unc-37/Groucho; ceh-30; transcriptional regulation] Supplemental material is available at http://www.genesdev.org.

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“…An ARID family TF CFI-1 (CEM neuron Fate Inhibition 1) binds to an AT rich region and is required for the CEM fate inhibition (Shaham and Bargmann 2002). However, cfi-1 is not required for pkd-2 expression in CEM neurons (Shaham and Bargmann 2002). Identifying the TFs that activate daf-19m, daf-19m direct targets, and PKD gene battery regulators will reveal how a cilium is specialized in form and function.…”

Section: Resultsmentioning

confidence: 99%

“…The CEM/IL2 enhancer sequences are AT enriched. An ARID family TF CFI-1 (CEM neuron Fate Inhibition 1) binds to an AT rich region and is required for the CEM fate inhibition (Shaham and Bargmann 2002). However, cfi-1 is not required for pkd-2 expression in CEM neurons (Shaham and Bargmann 2002).…”

Section: Resultsmentioning

confidence: 99%

“…The axonemes of the PKD and IL2 neurons are similar in that they possess singlet microtubules of varying numbers, which are distinct from axonemes of the core amphid and phasmid neurons. Although the PKD and IL2 neurons have several features in common, they are also individually specified via distinct lineagedriven mechanisms and express different sets of neurotransmitters and neuropeptides (Lints and Emmons 1999;Nathoo et al 2001;Shaham and Bargmann 2002;Lints et al 2004;Peden et al 2007;Schwartz and Horvitz 2007). This raises the question of how the shared traits of PKD and IL2 neurons are patterned and how the PKD gene battery is regulated to generate functional sensory cilia.…”

mentioning

confidence: 99%

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Functional Specialization of Sensory Cilia by an RFX Transcription Factor Isoform

2010

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In animals, RFX transcription factors govern ciliogenesis by binding to an X-box motif in the promoters of ciliogenic genes. In Caenorhabditis elegans, the sole RFX transcription factor (TF) daf-19 null mutant lacks all sensory cilia, fails to express many ciliogenic genes, and is defective in many sensory behaviors, including male mating. The daf-19c isoform is expressed in all ciliated sensory neurons and is necessary and sufficient for activating X-box containing ciliogenesis genes. Here, we describe the daf-19(n4132) mutant that is defective in expression of the sensory polycystic kidney disease (PKD) gene battery and male mating behavior, without affecting expression of ciliogenic genes or ciliogenesis. daf-19(n4132) disrupts expression of a new isoform, daf-19m (for function in male mating). daf-19m is expressed in malespecific PKD and core IL2 neurons via internal promoters and remote enhancer elements located in introns of the daf-19 genomic locus. daf-19m genetically programs the sensory functions of a subset of ciliated neurons, independent of daf-19c. In the male-specific HOB neuron, M acts downstream of the zinc finger TF EGL-46, indicating that a TF cascade controls the PKD gene battery in this cell-type specific context. We conclude that the RFX TF DAF-19 regulates ciliogenesis via X-box containing ciliogenic genes and controls ciliary specialization by regulating non-X-box containing sensory genes. This study reveals a more extensive role for RFX TFs in generating fully functional cilia.

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Control of neuronal subtype identity by the C. elegans ARID protein CFI-1

Cited by 45 publications

References 55 publications

C. elegans ced-13 can promote apoptosis and is induced in response to DNA damage

C. elegans ced-13 can promote apoptosis and is induced in response to DNA damage

Control of sex-specific apoptosis in C. elegans by the BarH homeodomain protein CEH-30 and the transcriptional repressor UNC-37/Groucho

Functional Specialization of Sensory Cilia by an RFX Transcription Factor Isoform

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