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

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

Lee, Sunkyung, Kim, Do Han, Ahnn, Joohong, 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."

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.

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.

Greenwald IS et al. (1990) Cell "Cell fates in C. elegans: in medias ras."

Greenwald IS, Broach JR

[Cell, 1990]

ras proteins play a central role in controlling cell proliferation in a variety of organisms and also appear to mediate specific developmental processes in certain cells. Nonetheless, how ras protein activity is regulated and how ras protein activation yields its biological effect have not been clearly defined in any metazoan. Now, Han and Sternberg (1990a) have found that a ras protein is encoded by the C. elegans let-60 gene. Since powerful classical and molecular genetic methods are available for C. elegans, this finding offers great promise for identifying components of the ras pathway and defining the nature of their interactions in this organism. In addition, the extensive literature on the biochemistry and genetics of ras function in other organisms should greatly facilitate translating genetic analysis of let-60 (Beitel et al., 1990; Han and Sternberg, 1990b) into detailed molecular models of cell fate determination.