Qi W et al. (2021) Nat Commun "Author Correction: The secreted endoribonuclease ENDU-2 from the soma protects germline immortality in C. elegans."

Xu F, Pfeifer D, Baumeister R, Zhao Q, Long L, Qi W, Gromoff EDV, Yang W, Maier W

[Nat Commun, 2021]

Correction to: Nature Communications 10.1038/s41467-021-21516-6, published online 24 February 2021.The original version of this Article contained an error in the author affiliation.Ralf Baumeister was incorrectly associated with Department of Hematology, Oncology and Stem Cell Transplantation, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany. He is associated with Bioinformatics and Molecular Genetics (Faculty of Biology), Albert-Ludwigs-University Freiburg, Germany Spemann Graduate School of Biology and Medicine (SGBM), Albert-Ludwigs-University Freiburg, Germany Center for Biochemistry and Molecular Cell Research (Faculty of Medicine), Albert-Ludwigs-University Freiburg, Germany Signalling Research Centers BIOSS and CIBSS, Albert-Ludwigs-University Freiburg, Germany This has now been corrected in both the PDF and HTML versions of the Article.

Zhao C et al. (1993) Worm Breeder's Gazette "Cloning of the lin-32 Gene"

Emmons SW, Zhao C

[Worm Breeder's Gazette, 1993]

Cloning of the lin-32 gene Connie Zhao and Scott W. Emmons, Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461

Hubbard EJA et al. (1994) Worm Breeder's Gazette "Genetic Analysis of sel-10."

Hubbard EJA, Greenwald IS

[Worm Breeder's Gazette, 1994]

Genetic analysis of sel-10 E. Jane Albert Hubbard and Iva Greenwald Department of Biochemistry and Molecular Biophysics and Howard Hughes Medical Institute, Columbia University, New York, New York, 10032

Emmons SW et al. (1994) Worm Breeder's Gazette "Strain Names for non-C. elegans Species."

Emmons SW, Fitch DHA, Leroi AM

[Worm Breeder's Gazette, 1994]

Strain names for non-C. elegans species Scott W. Emmonst, Armand Leroit, and David Fitch, Department of Molecular Genetics, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, Department of Biology, New York University, RmlOO9 Main Bldg., Washington Square, New York, NY 10003

Po MD et al. (2012) Neuron "Releasing the inner inhibition for axon regeneration."

Po MD, Calarco JA, Zhen M

[Neuron, 2012]

The adult mammalian central nervous system exhibits restricted regenerative potential. Chen etal. (2011) and El Bejjani and Hammarlund (2012) used Caenorhabditis elegans to uncover intrinsic factors that inhibit regeneration of axotomized mature neurons, opening avenues for potential therapeutics.

Hall DH et al. (1994) Worm Breeder's Gazette "Cytology of Degenerin-Induced Cell Death in the PVM Neuron"

Driscoll MA, Chalfie M, Gu GQ, Hall DH, Gong L

[Worm Breeder's Gazette, 1994]

Cytology of degenerin-induced cell death in the PVM neuron David H. Hall, Guoqiang Gu+, Lei Gong#, Monica Driscoll#, and Martin Chalfie+, * Dept. Neuroscience, Albert Einstein College of Medicine, Bronx, N.Y. 10461 + Dept. Biological Sciences, Columbia University, New York, N.Y. 10027 # Dept. Molecular Biology and Biochemistry, Rutgers University, Piscataway, N.J. 08855

Silverstein NJ et al. (2017) Immunity "Interleukin-17: Why the Worms Squirm."

Huh JR, Silverstein NJ

[Immunity, 2017]

IL-17 is a cytokine known primarily for its role in inflammation. In a recent issue of Nature, Chen etal. (2017) demonstrate that IL-17 plays a neuromodulatory role in Caenorhabditis elegans by acting directly on neurons to amplify neuronal responses to stimuli and produce changes in animal behavior.

Artan M et al. (2016) Dev Cell "Heat FLiPs a Hormonal Switch for Longevity."

Lee SV, An SW, Artan M

[Dev Cell, 2016]

Temperature-sensing neurons in C.elegans reduce the life-shortening effects of high temperatures via steroid signaling. In this issue of Developmental Cell, Chen etal. (2016) elucidate the underlying mechanisms by which the transcription factor CREB induces the neuropeptide FLP-6 in the temperature-sensing neurons to counteract the life-shortening effects of high temperature.

Allen, Parker et al. (2021) International Worm Meeting "Role of the conserved cholinesterase family member CEST-1.1 and its modular metabolite products in life span control"

Curtis, Brian, Kruempel, Joseph, Hu, Patrick, Wrobel, Chester, Allen, Parker, Schroeder, Frank, Higgins-Chen, Albert

[International Worm Meeting, 2021]

Although the role of the C. elegans FoxO transcription factor DAF-16 in promoting longevity is well established, how DAF-16/FoxO extends life span remains poorly understood. While the identities of thousands of DAF-16/FoxO target genes are known, mechanistic links between DAF-16/FoxO-dependent regulation of specific genes and DAF-16/FoxO-dependent life span extension are lacking. We have discovered that a conserved cholinesterase family member encoded by the DAF-16/FoxO target gene cest-1.1 is required for full life span extension in the context of reduced DAF-2 insulin-like signaling and sufficient to extend life span when expressed in a wild-type background. A functional CEST-1.1::GFP fusion protein is expressed specifically in the intestine and localizes to the apical plasma membrane. Comparative metabolomic analysis using HPLC-high resolution mass spectrometry revealed that CEST-1.1 is required for the biosynthesis of two structurally novel nucleoside-like ascarosides termed uglas#1 and uglas#11. These surprising findings support a role for an unprecedented class of metabolites in life span control and orthogonally expand the landscape of biogenic small molecules that may influence aging.

Akin O et al. (2014) Cell "The shape of things to come."

Akin O, Zipursky SL

[Cell, 2014]

Surface receptors can link binding of ligands to changes in the actin-based cell cytoskeleton. Chia etal. and Chen etal. provide evidence for direct binding between the cytoplasmic tails ofreceptorsand the WAVE complex, a regulator of the actin nucleator Arp2/3 complex, which mighthelp to explain how environmental signals are translated into changes in morphology andmotility.