Hengartner, Michael (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "to be announced"

Hengartner, Michael

[C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany, 2010]

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Hengartner MO et al. (1992) Worm Breeder's Gazette "unc-50, a Gene Required for Acetylcholine Receptor Function, Encodes an Unfamiliar Protein"

Horvitz HR, Tsung N, Hengartner MO, Lewis JA

[Worm Breeder's Gazette, 1992]

unc-50, a gene requiired for acetylcholine receptor function, encodes an unfamiliar protein Michael Hengartner, Nancy Tsung, Jim Lewist, and Bob Horvitz HHMI, Dept. Biology, MIT, Cambridge, MA 02139, USA. t Division of Life Sciences, U. of Texas at San Antonio, San Antonio, IX 78249

Colonnello A et al. (2020) Neurotox Res "Correction to: Comparing the Neuroprotective Effects of Caffeic Acid in Rat Cortical Slices and Caenorhabditis elegans: Involvement of Nrf2 and SKN-1 Signaling Pathways."

Tunez I, Rubio-Lopez LC, Aguilera-Portillo G, Silva-Palacios A, Evaristo-Priego Y, Santamaria A, Galvan-Arzate S, Cortez-Nunez S, Aschner M, Rangel-Lopez E, Chen P, Colonnello A, Robles-Banuelos B, Garcia-Contreras R

[Neurotox Res, 2020]

One of the authors has incorrect family name spelling in the original article_. Michael Ashner should read as Michael Aschner.

Gysi, Stephan et al. (2011) International Worm Meeting "Axon guidance defects displayed by zfp-1 and lin-35 mutants depend on the presence of the transgene oxIs12."

Gysi, Stephan, Hengartner, Michael

[International Worm Meeting, 2011]

Heparan sulfate proteoglycans (HSPGs) are known in different organisms to influence a wide variety of signaling pathways. We previously showed that the HSPG core protein Syndecan (SDN-1) plays an important role during nervous system development. With the aim to find new components in HSPG related signaling processes influencing guidance of commissural axon of the D-type motor neurons we designed a forward genetic screen. One of the candidates of this screen, op481, mapped to a region not containing any previously characterized axon guidance gene. Molecular analysis revealed that op481 is a premature stop codon mutation in the gene zfp-1. Surprisingly we observed that the axon guidance defects of the sdn-1(zh20); zfp-1(ok554) double mutant were only visible if the D-type motor axons were labeled with the oxIs12[unc-47::gfp; lin-15+] transgene. Combined with one of the two other transgenes (oxIs268[unc-47::gfp] or juIs76[unc-25::gfp; lin-15+]) labeling the same neurons, the sdn-1(zh20); zfp-1(ok554) double mutant failed to show increased axon guidance defects. Interestingly we observed the very same phenomenon in animals carrying a mutation in lin-35: animals with the genotype lin-35(n745); sdn-1(zh20) oxIs12 showed axon guidance defects while lin-35(n745); sdn-1(zh20) double mutants failed to show defects in combination with oxIs268 or juIs76. Our efforts to shed light on this effect indicated that the site of integration of oxIs12 is the relevant difference. Using data from a whole genome sequencing approach of animals carrying oxIs12, we were able to localize the precise place of integration of oxIs12 at the very end of the 3'UTR of the gene grd-1 on the X chromosome. Furthermore, from the number of sequencing reads covering the transgene sequence we were able to roughly estimate the size of oxIs12 to about 3.6Mb. We are currently trying to find a satisfying answer to why oxIs12 is influencing axon guidance in zfp-1 and lin-35 mutants.

Xiong, Lei et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Involvement of a food sensing signaling, the DAF-2 signaling pathway, in the clearance of germ cell corpses"

Hengartner, Michael, Xiong, Lei

[C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany, 2010]

During both development and stress response, many C.elegans hemaphrodite germ cells die by apoptosis, which is followed by a rapid engulfment and subsequent phagocytosis of apoptotic cells. Many components required for the clearance of germ cell corpses are known. However, the physiological meaning of germ cell phagocytosis is unknown. One hypothesis is that worms could exploit germ cell corpses for fuel when food is limited. Here we report that a DAF-2/AGE-1/PDK-1-dependent but DAF-16-independent singaling pathway is involved in the regulation of phagocytosis of germ cell corpses. In these food sensing mutants, the clearance of apoptotic germ cells both after DNA damage and during development is much faster. Both daf-2 mutation and daf-2 RNAi feeding reduced the number of germ cell corpses after irradiation or during development. Furthermore, phagocytosis in soma was not affected in daf-2 mutant. Unexpectedly, engulfment mutations could suppress the reduction of germ cell corpses in daf-2 mutant, indicating DAF-2 signaling negatively regulates the degradation of apoptotic germ cells. Further experiments showed that daf-2 signaling inhibits the clearance of germ cell corpses in intestine but not in neuronal cells. We are now in the way to investigate how this faster phagocytosis of germ cell corpses in daf-2 mutants is linked to energy homeostasis. Our findings imply that worms have adapted a mechanism to exploit the germ cell corpses for maintaing energy upon food restriction.

Keller, Martin et al. (2013) International Worm Meeting "Post-transcriptional control of C. elegans germ cell apoptosis by RNA-binding proteins."

Hengartner, Michael O., Keller, Martin

[International Worm Meeting, 2013]

Post-transcriptional control of mRNAs by RNA-binding proteins (RBPs) has a prominent role in the regulation of gene expression. RBPs interact with mRNAs to control their biogenesis, splicing, transport, localization, translation and stability. Defects in such regulation can lead to a wide range of human diseases from neurological disorders to cancer. Many fundamental biological pathways related to such disorders are conserved between Caenorhabditis elegans and humans. Therefore, studying RBPs associated with apoptosis in C. elegans could potentially give insight into processes underlying human diseases. Several RBPs are known to regulate apoptosis in the adult C. elegans germline. How these RBPs control apoptosis is however largely unknown. To gain a more comprehensive understanding of the general involvement of RBPs in the regulation of germ cell apoptosis, we performed an RNAi screen to identify novel RBP candidates that affect germ cell death. We verified our RNAi results via loss-of-function mutants and focus on the following confirmed candidates: glh-1, wago-4 and wago-5. In order to understand how these RBPs control apoptosis, the target mRNAs and the RNA-binding motifs will be identified with the recently developed in-vivo PAR-CLIP technique. Furthermore, RBP-protein interaction will be dissected using co-immunoprecipitation experiments. Our approach will allow us to build up a model of the germ cell apoptosis RNA regulon and broaden our understanding on how RBPs orchestrate cellular events.

Zeng, Sheng et al. (2011) International Worm Meeting "A genetic screen for modulators of apoptosis and engulfment in C. elegans."

Hengartner, Michael O., Zeng, Sheng

[International Worm Meeting, 2011]

C. elegans has been used extensively for the study of the molecular mechanisms that control apoptosis and the clearance of apoptotic cells. We and others have previously shown that when cells are placed on the verge of apoptotic death, modulation of the engulfment signaling cascade that affect the extent of cell death: loss of engulfment signaling increases the fraction of cells that survive, whereas overactivation of engulfment signaling reduces cell survival. In order to identify new genes involved in the control of apoptosis, of cell corpse clearance, or in the cross-talk between these two pathways, we performed EMS screen for mutations that alter the number of surviving Pn.aap descendents in a ced-3(rf) background. We identified over 17 independent mutations with reduced Pn.aap cell numbers and over 6 independent mutations that with increased number of Pn.aap cells. Genome-wide sequencing identified candidate loci for several of these mutations. We are in the process of confirming the involvement of the identified genes in Pn.aap survival. We are particularly interested in the mutations with reduced Pn.aap numbers, as these might identify novel cell survival factors.

Holway AH et al. (2007) J Cell Biol "Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos"

Kim SH, Michael WM, La Volpe A, Holway AH

[J Cell Biol, 2007]

After publication of this manuscript, the authors noticed that two images (Fig. 4 B, top left and middle) had been duplicated from a previous publication (Holway, A.H., C. Hung, and W.M. Michael. 2005. Genetics. 169:14511460). Here we provide new images corresponding to these control experiments. The authors apologize for this oversight.

Howard RM et al. (2002) Genes Dev "C. elegans EOR-1/PLZF and EOR-2 positively regulate Ras and Wnt signaling and function redundantly with LIN-25 and the SUR-2 Mediator component."

Howard RM, Sundaram MV

[Genes Dev, 2002]

Due to a production error, the origin of the eor-1 and eor-2 gene names was printed without proper attribution. The eor genes have been independently identified by multiple groups, and eor stands for egl-1 suppressor (M. Hengartner, pers. comm.)/plasmid DiO uptake defective (M. Herman, pers. comm.)/raf enhancer (our work). We apologize for the oversight.

Zhou MH et al. (1996) Worm Breeder's Gazette "Liquid Culture of the Worms with a Fermentor"

Zhou MH, Yang H, Walthall WW

[Worm Breeder's Gazette, 1996]

The yield of C. elegans and their food (E.coli) are relatively low in the large liquid cultures growth (Koelle et al.,1994) and the whole growth process is tedious. Here we report the successful growth of C.elegans with a fermentor. The following protocol is based on the protocol by Michael Koelle and Tory Herman (1994) from Internet.