α-actinin is required for the proper assembly of Z-disk/focal-adhesion-like structures and for efficient locomotion in Caenorhabditis elegans.

The actin binding protein α-actinin is a major component of focal adhesions found in vertebrate cells and of focal-adhesion-like structures found in the body wall muscle of the nematode Caenorhabditis elegans. To study its in vivo function in this genetic model system, we isolated a strain carrying a deletion of the single C. elegans α-actinin gene.

Whole-genome profiling of mutagenesis in Caenorhabditis elegans.

Deep sequencing offers an unprecedented view of an organism's genome. We describe the spectrum of mutations induced by three commonly used mutagens: ethyl methanesulfonate (EMS), N-ethyl-N-nitrosourea (ENU), and ultraviolet trimethylpsoralen (UV/TMP) in the nematode Caenorhabditis elegans. Our analysis confirms the strong GC to AT transition bias of EMS.

Towards a mutation in every gene in Caenorhabditis elegans.

The combined efforts of the Caenorhabditis elegans Knockout Consortium and individuals within the worm community are moving us closer to the goal of identifying mutations in every gene in the nematode C. elegans. At present, we count about 7000 deletion alleles that fall within 5500 genes.

An intracellular serpin regulates necrosis by inhibiting the induction and sequelae of lysosomal injury.

Extracellular serpins such as antithrombin and alpha1-antitrypsin are the quintessential regulators of proteolytic pathways. In contrast, the biological functions of the intracellular serpins remain obscure. We now report that the C.

C. elegans deletion mutant screening.

The methods used by the Caenorhabditis elegans Gene Knockout Consortium are conceptually simple. One does a chemical mutagenesis of wild-type C. elegans, and then screens the progeny of the mutagenized animals, in small mixed groups, using polymerase chain reaction (PCR) to identify populations with animals where a portion of DNA bounded by the PCR primers has been deleted.