Simmons, Alicia N et al. (2009) International Worm Meeting "Analysis of mortal germline Mutants."

Godwin, Masa, Ahmed, Shawn, Simmons, Alicia N, Liu, Yan, Hedges, Ashley, Nakashima, Aisa

[International Worm Meeting, 2009]

A number of C. elegans mutants that posses a mortal germline phenotype have been isolated. These mutants suffer from heritable forms of damage. To gain a better understanding of the nature of the processes that promote germ cell immortality, genetic and phenotypic analysis of mortal germline mutants is being performed. Of the mutants examined thus far, all occur as a consequence of single recessive mutations. Further characterization of the genetic underprimings of these mutants, and their effects on germ cell development will be presented.

Hiroyuki Sasakura et al. (2002) Japanese Worm Meeting "Isolation and analysis of mutants defective in AFD thermosensory neuron development"

Atsushi Kuhara, Hitoshi Inada, Ikue Mori, Hiroyuki Sasakura

[Japanese Worm Meeting, 2002]

The AFD sensory neurons play a critical role in thermosensation of C. elegans . To isolate genes required for development of AFD thermosensory neurons, we have screened 600,000 mut-7 animals that carry AFD and AIY specific GFP markers. We found over a dozen mutants that are categorized into the following groups. The first group consists of nj11 mutant. In nj11 mutant, ttx-1 , a master gene for AFD specification is ectopically expressed in ASI. We found that ASI chemosensory neurons are transformed to be AFD thermosensory neurons at the level of both morphology and function in nj11 mutant. These result suggest that the gene mutated in nj11 mutant is normally required for ASI cell fate decision by repressing ttx-1 activity that is capable of inducing AFD thermosensory neuron development. nj11 mutation maps to the +20.1 - +27.1 interval on V. The second group of mutants include nj12 and other two mutants. Axon extensions are defective in these mutants. After entering the nerve ring, pre-mature termination of axons occurs within the ring. Movement of nj12 is normal, but other two mutants show UNC phenotype. nj12 mutation maps on I. The third group of mutants include nj13 and other nine mutants. Cell body positions of AFD and AIY are mislocalized in these mutants. Although the normal position of AFD cell body is posterior to the nerve ring, AFD cell bodies are anterior to the nerve ring in nj13 mutant. Also, AIY cell bodies are sometimes mislocalized, for example, they are localized on the dorsal side. We cloned this gene by transposon display and found that the gene encodes C. elegans homologue of L1CAM. L1CAM is neural cell adhesion molecule that is highly expressed in mammalian brain. In humans, mutations in L1CAM are associated with a neurological syndrome, such as MASA and CRASH. Our result suggest that C. elegans L1CAM is required for proper positioning of neurons.