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HIM-8 Binds to the X Chromosome Pairing Center and Mediates Chromosome-Specific Meiotic Synapsis
Surprisingly, a point mutation in him-8 that retains both chromosome binding and NE localization fails to stabilize pairing or promote synapsis, indicating that stabilization of homolog pairing is an active process in which the tethering of chromosome sites to the NE may be necessary but is not sufficient. Expand
Crossover distribution and high interference for both the X chromosome and an autosome during oogenesis and spermatogenesis in Caenorhabditis elegans.
Despite an increased frequency of nonrecombinant chromosomes, segregation of a nonreCombinant autosome during spermatogenesis appears to occur normally, indicating that an achiasmate segregation system helps to ensure faithful disjunction of autosomes during sPermatogenesis. Expand
DPY-26, a Link Between Dosage Compensation and Meiotic Chromosome Segregation in the Nematode
The DPY-26 protein is required in the nematode Caenorhabditis elegans for X-chromosome dosage compensation as well as for proper meiotic chromosome segregation. DPY-26 was shown to mediate both… Expand
Crossover Distribution and Frequency Are Regulated by him-5 in Caenorhabditis elegans
Although him-5 mutants are defective in segregation of the X chromosome, HIM-5 protein localizes preferentially to the autosomes, allowing us to begin to establish pathways for the control of crossover distribution and frequency. Expand
Suppression and function of X-linked lethal and sterile mutations in Caenorhabditis elegans.
The collection of recessive lethal and sterile mutants in the region of the X chromosome balanced by mnDp1(X;V) is expanded, with a total of 54 mutants, nine of which are hermaphrodite-sterile and nine are maternally influenced mutants, producing inviable zygote progeny. Expand
Sex determination and dosage compensation: lessons from flies and worms.
The study of sex determination and dosage compensation is providing more general lessons about different types of signaling pathways used to control alternative developmental states of cells and organisms. Expand
An acetylcholinesterase-deficient mutant of the nematode Caenorhabditis elegans.
- C. Johnson, J. G. Duckett, J. Culotti, R. K. Herman, P. Meneely, R. L. Russell
- Biology, Medicine
- 1 February 1981
Within a set of five separable molecular forms of acetylcholinesterase found in the nematode Caenorhabditis elegans, previously reported differences in kinetic properties identify two classes, A and B, likely to be under separate genetic control, a screening procedure was devised to search for mutants affected only in class A forms. Expand
Lethals, steriles and deficiencies in a region of the X chromosome of Caenorhabditis elegans.
Twenty-one X-linked recessive lethal and sterile mutations balanced by an unlinked X-chromosome duplication have been identified following EMS treatment of the small nematode, Caenorhabditis elegans.… Expand
Multiple sites of action of volatile anesthetics in Caenorhabditis elegans.
- P. Morgan, M. Sedensky, P. Meneely
- Biology, Chemistry
- Proceedings of the National Academy of Sciences…
- 1 April 1990
The simplest explanation of the observations is that volatile anesthetics cause immobility in C. elegans by specifically interacting with multiple sites, which is in turn more consistent with involvement of protein at the site(s) of action. Expand
Genetic analysis of halothane sensitivity in Caenorhabditis elegans.
The nematode Caenorhabditis elegans appears to be a useful model for studying the action of volatile anesthetics and results show that sensitivity to halothane can be altered by mutations in several different genes. Expand