Han H-P et al. (1992) Worm Breeder's Gazette "Expression and Localization of the cha-1 and unc-17 Gene Products"

Rand JB, Duerr JS, Han H-P

[Worm Breeder's Gazette, 1992]

EXPRESSION AND LOCALIZATION OF THE cha-l AND unc-17 GENE PRODUCTS He-ping Han, Janet Duerr, and Jim Rand, Oklahoma Medlcal Research Foundation, Oklahoma Clty, OK 73104

Simske JS et al. (1994) Worm Breeder's Gazette "Specification of Vulval Cell Fates By Sequential Signalling Pathways."

Simske JS, Kim SK

[Worm Breeder's Gazette, 1994]

Specification of vulval cell fates by sequential signaling pathways Jeffrey S. Simske and Stuart K. Kim, Dept. of Developmental Biology, Stanford University Medical Center, Stanford CA 94305

Tomoyo Hamada et al. (2001) International C. elegans Meeting "Tissue localization and epitope-based functional analysis of the ryanodine receptor of Caenorhabditis elegans"

Yasuji Sakube, Do Han Kim, Hiroaki Kagawa, Joohong Ahnn, Tomoyo Hamada

[International C. elegans Meeting, 2001]

Muscle contraction is triggered by the release of Ca 2+ from the sarcoplasmic reticulum (SR) via a Ca 2+ release channel which is known as the ryanodine receptor. The ryanodine receptor of C. elegans (CeRyR) is encoded by a single unc-68 gene, which is composed of 5,071 amino acids. Although the knockout mouse of skeletal or cardiac RyR is lethal, the unc-68 null mutants show weak Unc and are viable. The unc-68(kh30) animals show intermittent convulsion before paralysis in anesthetic ketamine solution. The kh30 mutation causes substitution of Ser1,444 to Asn, at a predictive phosphorylation site of protein kinase C. To know the detail localization and functional domains of CeRyR, we made the fusion proteins of the putative functional regions in CeRyR and raised antiserum against them. We have obtained the region-specific antibodies of CeRyR by affinity purification of antiserum. Only one antibody against the region corresponding to the kh30 mutation site was useful for immunostaining. CeRyR was found to be located in body wall, pharyngeal, vulval, enteric and sex muscles, but not in neurons and intestine. We confirmed that CeRyR was present in muscles of the kh30 animal but not in those of unc-68 null mutants. CeRyR was expressed from comma stage as well as myofilament components. The expression at comma stage was weak but strongly from 1-1/2 fold. Ca 2+ bound to the regions of two EF-hand motifs and the C-terminal. Calsequestrin (CSQ-1) which is Ca 2+ binding protein in SR could not bind CeRyR directly. On the basis of these results, we propose a model based on the functional domains of CeRyR. Our model agrees well with a model based on the results of proteolysis and cross-linking analyses of mammalian skeletal RyR. It suggests that CeRyR may be a primitive RyR and is useful for analysis of the function of the ryanodine receptor not only C. elegans but also in other animals.

Roque CG et al. (2018) Neuron "Wimpy Nerves: piRNA Pathway Curbs Axon Regrowth after Injury."

Roque CG, Hengst U

[Neuron, 2018]

While PIWI-interacting RNAs (piRNAs) are primarily recognized as guardians of genome integrity, new functions of these small non-coding RNAs are emerging. In this issue, Kim etal. (2018) describe a piRNA-based mechanism that limits axon regeneration in C.elegans.

Peter Swoboda et al. (2002) European Worm Meeting "A multifaceted approach to elucidate the regulation of ciliogenesis in C. elegans"

Evgeni Efimenko, Peter Swoboda

[European Worm Meeting, 2002]

Cilia are evolutionarily conserved subcellular organelles functioning in cell motility, movement of extracellular fluids, sensory perception (e.g. smell) and determination of left-right asymmetry. While a great deal is known about the structure, function and motility of cilia, very little is known about the molecular mechanisms that regulate ciliogenesis in a cell-type specific and developmental manner. How do cilia become functional? How can they do what they do?

Gruber J et al. (2017) Cell "Microbiome and Longevity: Gut Microbes Send Signals to Host Mitochondria."

Kennedy BK, Gruber J

[Cell, 2017]

The microbiome has emerged as a major determinant of the functioning of host organisms, affecting both health and disease. Here, Han etal. use the workhorse of aging research, C.elegans, to identify specific mechanisms by which gut bacteria influence mitochondrial dynamics and aging, a first steptoward analogous manipulations to modulate human aging.

Gunasekaran Singaravelu et al. (2008) ""Pleiotropic roles of a Calcium binding protein, Calumenin in Caenorhabditis elegans""

Do Han Kim, Gunasekaran Singaravelu, Soonjae Kwon, Hyun-Ok Song, Weixun Li, Joohong Ahnn

[2008]

"Calumenin is calcium binding protein containing EF hand motif. It is localized in the ER. Perturbed level of calumenin is casually associated with several diseases such as cancer, atherosclerosis and drug resistance. However, the physiological role of calumenin is largely unknown. Caenorhabditis elegans calumenin shows 45% identity and 62% similarity with its human counterpart. We have characterized a deletion mutant of C. elegans calumenin, calu-1(tm1783), in which approximately 200bp of 5 upstream region followed by the initial two exons are deleted. Western blot and RT-PCR showed that it is a loss-of-function mutant. Around 37% of the mutants showed bursted vulva phenotype during the transition from L4 to adult molt. Furthermore, mutants exhibit pleiotropic defects such as decreased brood size, sluggish locomotion, small body size, slow growth, suggesting calumenin is important for normal development in C. elegans. We found that, in male, calumenin has strong expression in pharynx, spicules."

Ashrafi K (2022) Cell Host Microbe "Better living through communal eating."

Ashrafi K

[Cell Host Microbe, 2022]

Caenorhabditis elegans do not grow on either Staphylococcus saprophyticus or heat-killed Escherichia coli, but do so when exposed to both. In this issue of Cell Host & Microbe, Geng and colleagues have identified E.coli-derived signals as well as the host's neural and innate immunity pathways that promote digestion of S.saprophyticus.

Irazoqui JE (2014) Cell Host Microbe "DAF-tly depart stinky situations with elegans."

Irazoqui JE

[Cell Host Microbe, 2014]

During acute infection our behavior tends to change. Despite how common sickness behavior is, its molecular basis is not well understood. In a study published in Cell, Kim and colleagues (Meisel etal., 2014) implicate bacterial secondary metabolites as triggers of neural TGF-? signaling, which results in behavioral change during infection.

Vader G et al. (2014) Dev Cell "HORMA domains at the heart of meiotic chromosome dynamics."

Musacchio A, Vader G

[Dev Cell, 2014]

HORMA domain proteins are required for the careful orchestration of chromosomal organization during meiosis. Kim et al. (2014) and Silva et al. (2014) now provide structural and functional insights into the roles of C. elegans HORMA proteins, revealing parallels to the function of the HORMA protein MAD2 in mitotic checkpoint signaling.