Guenther C et al. (1996) Development "Asymmetric distribution of the C. elegans HAM-1 protein in neuroblasts enables daughter cells to adopt distinct fates."

Garriga G, Guenther C

[Development, 1996]

One mechanism of generating cellular diversity is to distribute developmental potential asymmetrically to daughter cells at mitosis. Two observations described in this report suggest that the C. elegans HAM-1 protein functions in dividing neuroblasts to produce daughter cells that adopt distinct fates. First, HAM-1 is asymmetrically distributed to the periphery of certain mitotic cells, ensuring that it will be inherited by only one daughter cell. Second, ham-1 mutations disrupt the asymmetric divisions of five neuroblasts. In one of these divisions, loss of ham-1 function causes the daughter cell that does not inherit HAM-1 to adopt the fate of the daughter cell that normally inherits HAM-1. We propose that asymmetric distribution of HAM-1 enables daughter cells to adopt distinct fates.

Garriga G et al. (1993) Genes Dev "Migrations of the Caenorhabditis elegans HSNs are regulated by egl-43, a gene encoding two zinc finger proteins."

Garriga G, Horvitz HR, Guenther C

[Genes Dev, 1993]

During embryonic development, the two Caenorhabditis elegans HSN motor neurons migrate from their birthplace in the tail to positions near the middle of the embryo. Here, we demonstrate that of all cells that undergo long-range migrations, only the HSNs are affected in animals that lack function of the egl-43 gene. We also show that egl-43 function is required for normal development of phasmid neurons, which are sensory neurons located in the tail. The egl-43 gene encodes two proteins containing zinc finger motifs that are similar to the zinc fingers of the murine Evi-1 proto-oncoprotein. Our genetic and molecular results suggest that egl-43 encodes two transcription factors and acts to control HSN migration and phasmid neuron development, presumably by regulating other genes that function directly in these processes.

Frank CA et al. (2005) Dev Biol "C. elegans HAM-1 positions the cleavage plane and regulates apoptosis in asymmetric neuroblast divisions."

Guenther C, Frank CA, Garriga G, Hawkins NC, Horvitz HR

[Dev Biol, 2005]

Asymmetric cell division occurs when a mother cell divides to generate two distinct daughter cells, a process that promotes the generation of cellular diversity in metazoans. During Caenorhabditis elegans development, the asymmetric divisions of neural progenitors generate neurons, neural support cells and apoptotic cells. C. elegans HAM-1 is an asymmetrically distributed cortical protein that regulates several of these asymmetric neuroblast divisions. Here, we show that HAM-1 is a novel protein and define residues important for HAM-1 function and distribution to the cell cortex. Our phenotypic analysis of ham-1 mutant embryos suggests that HAM-1 controls only neuroblast divisions that produce apoptotic cells. Moreover, ham-1 mutant embryos contain many unusually large cell-death corpses. An investigation of this corpse phenotype revealed that it results from a reversal of neuroblast polarity. A misplacement of the neuroblast cleavage plane generates daughter cells of abnormal size, with the apoptotic daughters larger than normal. Thus, HAM-1 regulates the position of the cleavage plane, apoptosis and mitotic potential in C. elegans asymmetric cell divisions.

Baum PD et al. (1999) Genes Dev "The Caenorhabditis elegans gene ham-2 links Hox patterning to migration of the HSN motor neuron."

Frank CA, Baum PD, Guenther C, Garriga G, Pham BV

[Genes Dev, 1999]

The Caenorhabditis elegans HSN motor neurons permit genetic analysis of neuronal development at single-cell resolution. The egl-5 Hox gene, which patterns the posterior of the embryo, is required for both early (embryonic) and late (larval) development of the HSN. Here we show that ham-2 encodes a zinc finger protein that acts downstream of egl-5 to direct HSN cell migration, an early differentiation event. We also demonstrate that the EGL-43 zinc finger protein, also required for HSN migration, is expressed in the HSN specifically during its migration. In an egl-5 mutant background, the HSN still expresses EGL-43, but expression is no longer down-regulated at the end of the cell's migration. Finally, we find a new role in early HSN differentiation for UNC-86, a POU homeodomain transcription factor shown previously to act downstream of egl-5 in the regulation of late HSN differentiation. In an unc-86; ham-2 double mutant the HSNs are defective in EGL-43 down-regulation, an egl-5-like phenotype that is absent in either single mutant. Thus, in the HSN, a Hox gene, egl-5, regulates cell fate by activating the transcription of genes encoding the transcription factors HAM-2 and UNC-86 that in turn individually control some differentiation events and combinatorially affect others.

Zhao Y et al. (2007) BMC Genomics "Poly-G/poly-C tracts in the genomes of Caenorhabditis."

Zhao Y, O'Neil NJ, Rose AM

[BMC Genomics, 2007]

ABSTRACT: BACKGROUND: In the genome of Caenorhabditis elegans, homopolymeric poly-G/poly-C tracts (G/C tracts) exist at high frequency and are maintained by the activity of the DOG-1 protein. The frequency and distribution of G/C tracts in the genomes of C. elegans and the related nematode, C. briggsae were analyzed to investigate possible biological roles for G/C tracts. RESULTS: In C. elegans, G/C tracts are distributed along every chromosome in a non-random pattern. Most G/C tracts are within introns or are close to genes. Analysis of SAGE data showed that G/C tracts correlate with the levels of regional gene expression in C. elegans. G/C tracts are over-represented and dispersed across all chromosomes in another Caenorhabditis species, C. briggase. However, the positions and distribution of G/C tracts in C. briggsae differ from those in C. elegans. Furthermore, the C. briggsae dog-1 ortholog CBG19723 can rescue the mutator phenotype of C. elegans dog-1 mutants. CONCLUSIONS: The abundance and genomic distribution of G/C tracts in C. elegans, the effect of G/C tracts on regional transcription levels, and the lack of positional conservation of G/C tracts in C. briggsae suggest a role for G/C tracts in chromatin structure but not in the transcriptional regulation of specific genes.

Antika TR et al. (2023) J Biol Chem "Sequence-specific targeting of C. elegans C-Ala to the D-loop of tRNAAla."

Horng JC, Hsu HL, Nazilah KR, Wang CC, Wang TL, Wang SC, Antika TR, Chuang TH, Chrestella DJ, Wang SW, Tseng YK, Pan HC

[J Biol Chem, 2023]

Alanyl-tRNA synthetase (AlaRS) retains a conserved prototype structure throughout its biology. Nevertheless, its C-terminal domain (C-Ala) is highly diverged and has been shown to play a role in either tRNA or DNA binding. Interestingly, we discovered that Caenorhabditis elegans cytoplasmic C-Ala (Ce-C-Ala_c) robustly binds both ligands. How Ce-C-Ala_c targets its cognate tRNA and whether a similar feature is conserved in its mitochondrial counterpart remain elusive. We show that the N- and C-terminal subdomains of Ce-C-Ala_c are responsible for DNA and tRNA binding, respectively. Ce-C-Ala_c specifically recognized the conserved invariant base G¹⁸ in the D-loop of tRNA^Ala through a highly conserved lysine residue, K934. Despite bearing little resemblance to other C-Ala domains, C. elegans mitochondrial C-Ala (Ce-C-Ala_m) robustly bound both tRNA^Ala and DNA and maintained targeting specificity for the D-loop of its cognate tRNA. This study uncovers the underlying mechanism of how C. elegans C-Ala specifically targets the D-loop of tRNA^Ala.

Guven K (1995) Journal of Thermal Biology "Differential expression of hsp70 proteins in response to heat and cadmium in Caenorhabditis elegans."

Guven K

[Journal of Thermal Biology, 1995]

1. The patterns of HSP70 expression induced in Caenorhabditis elegans by mild (31 degrees C) or severe (34 degrees C) heat shock, and by cadmium ions at 31 degrees C, have been compared with those expressed constitutively ill 20 degrees C controls by 1- and a-dimensional immunoblotting. 2. The 2D spot patterns become more complex with increasing severity of stress (34 degrees C > 31 degrees C + Cd > 31 degrees C > 20 degrees C). 3. A stress-inducible transgene construct is minimally active at 31 degrees C, but is abundantly expressed in the presence of cadmium or at 34 degrees C. 4. Differing degrees or types of stress may differentially induce available hsp70

Xu J et al. (2018) J Nanosci Nanotechnol "Carbon Quantum Dots as Fluorescent Probes for Imaging and Detecting Free Radicals in C. elegans."

Wang Q, Guan S, Wang L, Wang M, Zhang Y, Mu Y, Xu J, Wang K, Li J

[J Nanosci Nanotechnol, 2018]

Uniform and hydrophilic carbon quantum dots (C-QDs) were synthesized by calcination and NaOH treatment from an organo-templated zeolite precursor. The color of luminescence was determined by the concentration of C-QDs. These variable-color C-QDs were applied for the first time in the imaging of Caenorhabditis elegans (C. elegans) as a model organism. The effects of C-QDs and possible behavioral changes in C. elegans were evaluated under treatment conditions. We could clearly observe distribution of C-QDs in C. elegans from the fluorescence images. Furthermore, we observed significant and detectable fluorescence quenching of the C-QDs by free radicals in C. elegans. Our work affirms that C-QDs can be developed as imaging probes and as potential fluorescent quantitative probes for detecting free radicals.

Lu L et al. (2021) Mol Immunol "Whole transcriptome analysis of schinifoline treatment in Caenorhabditis elegans infected with Candida albicans."

Shu C, Ma S, Li S, Li Z, Shan C, Chen G, Lu L, Nie W, Wang H

[Mol Immunol, 2021]

Candida albicans is an opportunistic fungal human pathogen that has been causing an increasing number of deaths each year. Due to the widespread use of broad-spectrum antibiotics and immunosuppressants, C. albicans resistance to these therapies has increased. Thus, natural plant inhibitors are being investigated for treating C. albicans infections. Schinifoline is a 4-quinolinone alkaloid with antibacterial, insecticidal, antitumor, and other biological activities. Here, we explored the effects of schinifoline on C. albicans in C. elegans and extracted RNA from uninfected C. elegans, C. elegans infected with C. albicans, and C. elegans infected with C. albicans and treated with 100 mg/l schinifoline. Our results showed that there were significant differences among the three groups. The GO and KEGG pathway analysis suggested that the pathogenicity of C. albicans to C. elegans was caused by abnormal protein function. Schinifoline regulates lysosomal pathway related genes that accelerate the metabolism and degradation of abnormal proteins, thereby inhibiting the negative effects of C. albicans in vivo. These findings advance our understanding of the molecular mechanisms underlying schinifoline inhibition of C. albicans.

Wang BB et al. (1993) Cell "A homeotic gene cluster patterns the anteroposterior body axis of C. elegans."

Wang BB, Kenyon CJ, Robinson NT, Chisholm AD, Austin JA, Mueller-Immergluck MM

[Cell, 1993]

In insects and vertebrates, clusters of Antennapedia class homeobox (HOM-C) genes specify anteroposterior body pattern. The nematode C. elegans also contains a small cluster of HOM-C genes, one of which has been shown to specify positional identity. Here we show that two additional C. elegans HOM-C genes also specify positional identity and that together these three HOM-C genes function along the anteroposterior axis in the same order as their homologs in other organisms. Thus, HOM-C-based pattern formation has been conserved in nematodes despite the many differences in morphology and embryology that distinguish them from other phyla. Each C. elegans HOM-C gene is responsible for a distinct body region; however, where their domains overlap, two HOM-C genes can act together to specify the fates of individual cells.