Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva-Formation: Part II: Species With a Central Vulva"

Sommer RJ, Sternberg PW

[Worm Breeder's Gazette, 1994]

Evolution of vulva-formation: Part II: Species with a central vulva Ralf J. Sommer & Paul W. Sternberg, California Institute of Technology, Division of Biology 156-29, Pasadena, CA 91125

Li WQ et al. (1992) Worm Breeder's Gazette "Characterization of the Axonal Guidance and Outgrowth gene Unc-33"

Shaw JE, Li WQ, Herman RK

[Worm Breeder's Gazette, 1992]

Characterization of the axonal guidance and outgrowth gene unc-33 W. Li, R. K. Herman and J. E. Shaw Department of Genetics and Cell biology, University of Minnesota, St Paul, MN 55108

Sommer RJ et al. (1994) Worm Breeder's Gazette "Evolution of Vulva Formation: Part IV: Variation in AC Position Can Cause a Shift of Vulva Formation Towards P(4-6).p."

Sternberg PW, Sommer RJ

[Worm Breeder's Gazette, 1994]

Evolution of vulva formation: Part IV: Variation in AC position can cause a shift of vulva formation towards p(4- 6).p Ralf J. Sommer & Paul W. Sternberg, HHMI & California Institute of Technology, Division of Biology 156-29, Pasadena, CA

Mains PE (1994) Worm Breeder's Gazette "Interactions Between mei-1 and the unc-116 Kinesin"

Mains PE

[Worm Breeder's Gazette, 1994]

Interactions Between mei-l and the unc-116 Kinesin Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada

Wissmann AK et al. (1994) Worm Breeder's Gazette "Characterization of the let-502 Gene"

Mains PE, Wissmann AK, McGhee JD

[Worm Breeder's Gazette, 1994]

Characterization of the let-502 gene Andreas Wissmann, James D. McGhee and Paul E. Mains, Dept. of Medical Biochemistry, University of Calgary, Calgary, Alberta, Canada T2N 4N1

McGhee JD (1987) Biochemistry "Purification and characterization of a carboxylesterase from the intestine of the nematode Caenorhabditis elegans."

McGhee JD

[Biochemistry, 1987]

The major intestinal esterase from the nematode Caenorhabditis elegans has been purified to essential homogeneity. Starting from whole worms, the overall purification is 9000-fold with a 10% recovery of activity. The esterase is a single polypeptide chain of Mr 60,000 and is stoichiometrically inhibited by organophosphates. Substrate preferences and inhibition patterns classify the enzyme as a carboxylesterase (EC 3.1.1.1), but the physiological function is unknown. The sequence of 13 amino acid residues at the esterase N- terminus has been determined. This partial sequence shows a surprisingly high degree of similarity to the N-terminal sequence of two carboxylesterases recently isolated from Drosophila mojavensis [Pen, J., van Beeumen, J., & Beintema, J. J. (1986) Biochem. J. 238, 691-699].

Michael A Miller et al. (2002) Mid-west Worm Meeting "An Eph Receptor Sperm-Sensing Control Mechanism for Oocyte Meiotic Maturation"

David Greenstein, Paul J Ruest, Steven K Hanks, Mary Kosinski, Michael A Miller

[Mid-west Worm Meeting, 2002]

During sexual reproduction in most animals, oocytes arrest in meiotic prophase and resume meiosis (meiotic maturation or M-phase entry) in response to sperm or somatic cell signals (1). Despite progress in delineating mitogen-activated protein kinase (MAPK) and CDK/cyclin activation pathways involved in meiotic maturation, it is less clear how these pathways are regulated at the cell surface. In Caenorhabditis elegans, oocytes and somatic gonadal sheath cells sense the presence of sperm in the reproductive tract and prepare for fertilization (2). When sperm are absent, oocytes arrest in meiotic prophase for days (2). Sperm promote oocyte M-phase entry and MAPK activation using the major sperm protein (MSP) as a signaling molecule (3). MSP also functions in sperm locomotion, playing a role analogous to actin (4). Thus during evolution, MSP has acquired extracellular signaling and intracellular functions for reproduction. We present multiple lines of evidence that the VAB-1 Eph receptor protein-tyrosine kinase and a somatic gonadal sheath cell-dependent pathway, defined by the POU-homeobox gene ceh-18, negatively regulate oocyte M-phase entry and MAPK activation. MSP antagonizes these inhibitory circuits, in part by binding VAB-1 on oocytes and sheath cells. Eliminating vab-1 and ceh-18 function removes the dependence of meiotic maturation and ovulation on the presence of sperm. Therefore, this meiotic control mechanism resembles a cell cycle checkpoint (5) and may confer a selective advantage to hermaphrodites and females by conserving metabolically costly oocytes when sperm are unavailable for fertilization. MSP-domain proteins are found throughout the metazoa, including six in the human genome, and may regulate contact-dependent ephrin/Eph receptor signaling pathways.

Michael A Miller et al. (2002) East Coast Worm Meeting "An Eph Receptor Sperm-Sensing Control Mechanism for Oocyte Meiotic Maturation"

Michael A Miller, David Greenstein, Paul J Ruest, Mary Kosinski, Steven K Hanks

[East Coast Worm Meeting, 2002]

During sexual reproduction in most animals, oocytes arrest in meiotic prophase and resume meiosis (meiotic maturation or M-phase entry) in response to sperm or somatic cell signals (1). Despite progress in delineating mitogen-activated protein kinase (MAPK) and CDK/cyclin activation pathways involved in meiotic maturation, it is less clear how these pathways are regulated at the cell surface. In Caenorhabditis elegans, oocytes and somatic gonadal sheath cells sense the presence of sperm in the reproductive tract and prepare for fertilization (2). When sperm are absent, oocytes arrest in meiotic prophase for days (2). Sperm promote oocyte M-phase entry and MAPK activation using the major sperm protein (MSP) as a signaling molecule (3). MSP also functions in sperm locomotion, playing a role analogous to actin (4). Thus during evolution, MSP has acquired extracellular signaling and intracellular functions for reproduction. We present multiple lines of evidence that the VAB-1 Eph receptor protein-tyrosine kinase and a somatic gonadal sheath cell-dependent pathway, defined by the POU-homeobox gene ceh-18, negatively regulate oocyte M-phase entry and MAPK activation. MSP antagonizes these inhibitory circuits, in part by binding VAB-1 on oocytes and sheath cells. Eliminating vab-1 and ceh-18 function removes the dependence of meiotic maturation and ovulation on the presence of sperm. Therefore, this meiotic control mechanism resembles a cell cycle checkpoint (5) and may confer a selective advantage to hermaphrodites and females by conserving metabolically costly oocytes when sperm are unavailable for fertilization. MSP-domain proteins are found throughout the metazoa, including six in the human genome, and may regulate contact-dependent ephrin/Eph receptor signaling pathways.

Murakami S et al. (1999) Curr Biol "Life extension and stress resistance in Caenorhabditis elegans modulated by the tkr-1 gene."

Johnson TE, Murakami S

[Curr Biol, 1999]

In this Brief Communication, which appeared in the 14 September 1998 issue of Current Biology, the UV dose was reported erroneously. The dose reported was 20 J/m2 but the actual dose used was 0.4 J/cm2. Also, the gene formally referred to as tkr-1 has since been renamed old-1 (overexpression longevity determination).

Ramos CG et al. (2014) J Bacteriol "Retraction for Ramos et al., MtvR is a global small noncoding regulatory RNA in Burkholderia cenocepacia."

Feliciano JR, da Costa PJ, Ramos CG, Grilo AM, Leitao JH

[J Bacteriol, 2014]

Volume 195, no. 16, p. 35143523, 2013. A number of problems related to images published in this paper have been brought to our attention. Figure 1D contains duplicated images in lanes S and LE, and Fig. 4D and 6B contain images previously published in articles in this journal and in Microbiology and Microbial Pathogenesis, i.e., the following: C. G. Ramos, S. A. Sousa, A. M. Grilo, J. R. Feliciano, and J. H. Leitao, J. Bacteriol. 193:15151526, 2011. doi:10.1128/JB.01374-11. S. A. Sousa, C. G. Ramos, L. M. Moreira, and J. H. Leitao, Microbiology 156:896908, 2010. doi:10.1099/mic.0.035139-0. C. G. Ramos, S. A. Sousa, A. M. Grilo, L. Eberl, and J. H. Leitao, Microb. Pathog. 48:168177, 2010. doi: 10.1016/j.micpath.2010.02.006. Therefore, we retract the paper. We deeply regret this situation and apologize for any inconvenience to the editors and readers of Journal of Bacteriology, Microbial Pathogenesis, and Microbiology.