The art and design of genetic screens: Caenorhabditis elegans

2002 ◽  
Vol 3 (5) ◽  
pp. 356-369 ◽  
Author(s):  
Erik M. Jorgensen ◽  
Susan E. Mango
Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 805-813 ◽  
Author(s):  
Edward S Davis ◽  
Lucia Wille ◽  
Barry A Chestnut ◽  
Penny L Sadler ◽  
Diane C Shakes ◽  
...  

Abstract Two genes, originally identified in genetic screens for Caenorhabditis elegans mutants that arrest in metaphase of meiosis I, prove to encode subunits of the anaphase-promoting complex or cyclosome (APC/C). RNA interference studies reveal that these and other APC/C subunits are essential for the segregation of chromosomal homologs during meiosis I. Further, chromosome segregation during meiosis I requires APC/C functions in addition to the release of sister chromatid cohesion.


2005 ◽  
Vol 6 (7) ◽  
pp. 557-567 ◽  
Author(s):  
Benjamin T. Kile ◽  
Douglas J. Hilton

2015 ◽  
Vol 5 (3) ◽  
pp. 467-475 ◽  
Author(s):  
Xiaoyin Chen ◽  
Margarete Diaz Cuadros ◽  
Martin Chalfie

Abstract Caenorhabditis elegans senses gentle touch along the body via six touch receptor neurons. Although genetic screens and microarray analyses have identified several genes needed for touch sensitivity, these methods miss pleiotropic genes that are essential for the viability, movement, or fertility of the animals. We used neuronally enhanced feeding RNA interference to screen genes that cause lethality or paralysis when mutated, and we identified 61 such genes affecting touch sensitivity, including five positive controls. We confirmed 18 genes by using available alleles, and further studied one of them, tag-170, now renamed txdc-9. txdc-9 preferentially affects anterior touch response but is needed for tubulin acetylation and microtubule formation in both the anterior and posterior touch receptor neurons. Our results indicate that neuronally enhanced feeding RNA interference screens complement traditional mutageneses by identifying additional nonviable genes needed for specific neuronal functions.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Brittany Rosener ◽  
Serkan Sayin ◽  
Peter O Oluoch ◽  
Aurian P García González ◽  
Hirotada Mori ◽  
...  

Metabolism of host-targeted drugs by the microbiome can substantially impact host treatment success. However, since many host-targeted drugs inadvertently hamper microbiome growth, repeated drug administration can lead to microbiome evolutionary adaptation. We tested if evolved bacterial resistance against host-targeted drugs alters their drug metabolism and impacts host treatment success. We used a model system of Caenorhabditis elegans, its bacterial diet, and two fluoropyrimidine chemotherapies. Genetic screens revealed that most of loss-of-function resistance mutations in Escherichia coli also reduced drug toxicity in the host. We found that resistance rapidly emerged in E. coli under natural selection and converged to a handful of resistance mechanisms. Surprisingly, we discovered that nutrient availability during bacterial evolution dictated the dietary effect on the host – only bacteria evolving in nutrient-poor media reduced host drug toxicity. Our work suggests that bacteria can rapidly adapt to host-targeted drugs and by doing so may also impact the host.


2008 ◽  
Vol 9 (3) ◽  
pp. 192-203 ◽  
Author(s):  
Héctor Candela ◽  
Sarah Hake

2003 ◽  
Vol 4 (6) ◽  
pp. 419-431 ◽  
Author(s):  
Howard A. Shuman ◽  
Thomas J. Silhavy

2020 ◽  
Vol 219 (5) ◽  
Author(s):  
Matthew E. Hurlock ◽  
Ivana Čavka ◽  
Lisa E. Kursel ◽  
Jocelyn Haversat ◽  
Matthew Wooten ◽  
...  

The synaptonemal complex (SC) is a tripartite protein scaffold that forms between homologous chromosomes during meiosis. Although the SC is essential for stable homologue pairing and crossover recombination in diverse eukaryotes, it is unknown how individual components assemble into the highly conserved SC structure. Here we report the biochemical identification of two new SC components, SYP-5 and SYP-6, in Caenorhabditis elegans. SYP-5 and SYP-6 are paralogous to each other and play redundant roles in synapsis, providing an explanation for why these genes have evaded previous genetic screens. Superresolution microscopy reveals that they localize between the chromosome axes and span the width of the SC in a head-to-head manner, similar to the orientation of other known transverse filament proteins. Using genetic redundancy and structure–function analyses to truncate C-terminal tails of SYP-5/6, we provide evidence supporting the role of SC in both limiting and promoting crossover formation.


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