Nemagenetag collection

In the framework of the European Union funded Nemagenetag project, several labs worked together from 2003 to 2007 to generate a genome-wide collection of molecularly characterized Mos1 insertion mutants for the C. elegans community. The relevance and utility of this collection of >13000 strains has been drastically reduced with the advent of CRISPR. Requests for strains have dropped to an average of less than one a month. The Nemagenetag members consider that the cost involved in maintaining the collection is no longer warranted. Any laboratory interested in the collection (available in duplicate) should contact us before 15th June. If there are no takers, we will dispose of the collection as we see fit.

We take this opportunity to remind you that if ever you use a Nemagenetag allele (“ttTi”, including MoSCI alleles such as ttTi5605) you should always cite the relevant publications. Without such citation, community projects will not get funding.

Vallin et al.
A genome-wide collection of Mos1 transposon insertion mutants for the C. elegans research community.
PLoS One. 2012;7(2):e30482. doi: 10.1371/journal.pone.0030482. Epub 2012 Feb 8.

Duverger et al.
A semi-automated high-throughput approach to the generation of transposon insertion mutants in the nematode Caenorhabditis elegans.
Nucleic Acids Res. 2007;35(2):e11. Epub 2006 Dec 12.
PMID: 17164286

Jonathan Ewbank on behalf of the Nemagenetag consortium

Latest chapter of WormBook in GENETICS: Programmed Cell Death During Caenorhabditis elegans Development

Check out the latest chapter of WormBook in GENETICS!

Programmed Cell Death During Caenorhabditis elegans Development
Barbara Conradt, Yi-Chun Wu, Ding Xue
GENETICS August 1, 2016 vol. 203 no. 4 1533-1562; DOI: 10.1534/genetics.115.186247

Programmed cell death is an integral component of Caenorhabditis elegans development. Genetic and reverse genetic studies in C. elegans have led to the identification of many genes and conserved cell death pathways that are important for the specification of which cells should live or die, the activation of the suicide program, and the dismantling and removal of dying cells. Molecular, cell biological, and biochemical studies have revealed the underlying mechanisms that control these three phases of programmed cell death. In particular, the interplay of transcriptional regulatory cascades and networks involving multiple transcriptional regulators is crucial in activating the expression of the key death-inducing gene egl-1 and, in some cases, the ced-3 gene in cells destined to die. A protein interaction cascade involving EGL-1, CED-9, CED-4, and CED-3 results in the activation of the key cell death protease CED-3, which is tightly controlled by multiple positive and negative regulators. The activation of the CED-3 caspase then initiates the cell disassembly process by cleaving and activating or inactivating crucial CED-3 substrates; leading to activation of multiple cell death execution events, including nuclear DNA fragmentation, mitochondrial elimination, phosphatidylserine externalization, inactivation of survival signals, and clearance of apoptotic cells. Further studies of programmed cell death in C. elegans will continue to advance our understanding of how programmed cell death is regulated, activated, and executed in general.