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

Han H-P, Duerr JS, Rand JB

[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."

Kim SK, Simske JS

[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

Lim, Yun-Ki et al. (2011) International Worm Meeting "Regulation of calreticulin gene expression by sumoylation in C. elegance."

Lee, Sunkyung, Ahnn, Joohong, Kim, Do Han, Lim, Yun-Ki

[International Worm Meeting, 2011]

Sumoylation is a reversible post-translational modification which is involved in diverse biological processes including protein stability, nuclear-cytosolic transport, DNA binding activity, and gene expression. In C.elegans, sumoylation has been shown to be critical in gonadal development by modulating chromatin integrity and transcription (Broday et al., Genes & Dev. 18, 2380 2004). Calreticulin is a calcium binding protein residing in endoplasmic reticulum that plays pivotal roles in calcium homeostasis, chaperone activity, and glycosylation and transcriptionally up-regulated by unfolded protein response (UPR) in C.elegans. In order to understand the role of sumoylation on the UPR response in nematode, we attempted to study the function of SUMO conjugating enzyme UBC-9 on calreticulin gene regulation. ubc-9 mutant worms showed defective vulval development similar to smo-1, lack of SUMO protein. We found that, upon abolishing sumoylation, GFP fluorescence driven by calreticulin promoter was increased in C. elegans. Furthermore, the increased GFP fluorescence was attenuated by knockdown of xbp-1, indicating that sumoylation is required for transcriptional repression of calreticulin in C. elegans. We are currently investigating underlying mechanism to elucidate how sumoylation controls gene expression of calreticulin in C.elegans.

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

Hengst U, Roque CG

[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"

Peter Swoboda, Evgeni Efimenko

[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."

Gruber J, Kennedy BK

[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.

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."

Vader G, Musacchio A

[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.

Song, Hyun-Ok et al. (2009) International Worm Meeting "Pleiotropic roles of a calcium binding protein, calumenin in C. elegans."

Singaravelu, Gunasekaran, Kim, Do Han, Ahnn, Joohong, Kwon, Soonjae Kwon, Dwivedi, Meenakshi, Sung, Hyun, Song, Hyun-Ok

[International Worm Meeting, 2009]

Calumenin is a Ca2+ binding protein located in the lumen of endoplasmic reticulum. Even though it has been implicated in various diseases, the in vivo functions of calumenin have not yet been reported. Here, we report the characterization of C. elegans calumenin loss of function mutant, calu-1(tm1783). Biochemical analysis revealed that CALU-1 binds with Ca2+ and the calu-1(tm1783) mutant exhibited pleiotropic defects such as decreased brood size, reduced egg laying rate, sluggish locomotion, and small body size suggesting the multiple roles of calumenin in C. elegans. Consistent to its ability to bind Ca2+, calu-1(tm1783) mutant shows reduced pumping rate and prolonged defecation cycle, which are known to be mediated by Ca2+ signaling in C. elegans. The knock-down of calu-1 phenocopies calu-1(tm1783) mutant, suggesting that specific loss of CALU-1 is responsible for the observed defects. Interestingly, calu-1(tm1783) mutant has severe defects in cuticle showing aberrant annuli and deformed alae indicating the possible role(s) of calumenin in cuticle formation and/or maintenance. To our knowledge, this is the first report of genetic analysis of calumenin illustrating its in vivo functions.