Functional and Genetic Analysis of VAB-10 Spectraplakin in Caenorhabditis elegans

Author(s):  
Christelle Gally ◽  
Huimin Zhang ◽  
Michel Labouesse
Genetics ◽  
1981 ◽  
Vol 99 (3-4) ◽  
pp. 415-428
Author(s):  
Raja E Rosenbluth ◽  
David L Baillie

ABSTRACT The Caenorhabditis elegans mutation e873, which results in a recessive uncoordinated phenotype (formerly named Unc-72) and which had been isolated after 32P t reatment (BRENNER1 974), has now been found to act as a crossover suppressor and to be associated with a translocation between linkage groups (LG's) IIIand V. The translocation has been named, eTl(ZI1; V); eT1acts as a dominant crossover suppressor for both the right half of LGIIIand the left half of LGV,providing a balancer for a total of 39 map units. The uncoordinated e873phenotype has been shown to be a consequence of Eminactive unr- 36111gene. It was possible to demonstrate that, in translocation heterozygotes, eT1chromosomes marked with either sma-3or dpy-11segregate from normal LGIII,while those marked with bli-5, sm-2or unc-42segregate from normal LGV.Since bli-5and sma-2are normally on LGIII,and dpy-11is normally on LGV,it is concluded that: (a) eT1is a reciprocal translocation; (b) there is a breakpoint between sma-3and sma-2in LGIII(the region containing unc- 36)and one between dpy-11and unc-42in LGV;(c) thera is no dominant centromere between sma-2and bli-5on LGIII,since in eT1these genes are not linked to a LGIIIcentromere. Similarly, it is highly unlikely that there is a centromere to the left of dpy-11on LGV.The new gene order in eT1was determined by measuring recombination rates between markers in eT1homozygotes. It is concluded that the new order is: dpy-1 sma-3 (break) dpy-11 unc-60,and bli-5 sma-2 (break) unc-42 unc-51.——Thisis the first analysis of a C. eleganstranslocation with respect to reciprocity, breakpoints and new gene order.


Nematology ◽  
2000 ◽  
Vol 2 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Marie Delattre ◽  
Marie-Laure Dichtel ◽  
Marie-Anne Félix

AbstractIn order to study the evolution of nematode vulva development, we focus on Oscheius/Dolichorhabditis sp. CEW1 (Rhabditidae) in comparison with Caenorhabditis elegans. In this species, the fates of the vulval precursor cells are determined by two successive nested inductions by the uterine anchor cell (instead of a single one in C. elegans). This hermaphroditic species can be cultured and handled like C. elegans. We review vulva development in this species. We present some molecular tools and the sequence of the Ras gene. This species is amenable to genetic analysis and we discuss the isolation of morphological markers. Afin d’étudier l’évolution du développement de la vulve des nématodes, nous nous concentrons sur l’espèce Oscheius/Dolichorhabditis sp. CEW1 (Rhabditidae) en la comparant à Caenorhabditis elegans. Dans cette espèce, les destinées des cellules précurseurs de la vulve sont déterminées par deux inductions emboîtées provenant de la cellule ancre de l’utérus (au lieu d’une seule chez C. elegans). Cette espèce hermaphrodite peut être élévée et manipulée comme C. elegans. Nous décrivons le développement de la vulve dans cette espèce. Nous présentons des outils moléculaires et la séquence du gène Ras. Les analyses génétiques sont possibles dans cette espèce et nous discutons l’isolement de marqueurs morphologiques.


2007 ◽  
Vol 18 (10) ◽  
pp. 3883-3893 ◽  
Author(s):  
Peter Juo ◽  
Tom Harbaugh ◽  
Gian Garriga ◽  
Joshua M. Kaplan

The proline-directed kinase Cdk5 plays a role in several aspects of neuronal development. Here, we show that CDK-5 activity regulates the abundance of the glutamate receptor GLR-1 in the ventral cord of Caenorhabditis elegans and that it produces corresponding changes in GLR-1–dependent behaviors. Loss of CDK-5 activity results in decreased abundance of GLR-1 in the ventral cord, accompanied by accumulation of GLR-1 in neuronal cell bodies. Genetic analysis of cdk-5 and the clathrin adaptin unc-11 AP180 suggests that CDK-5 functions prior to endocytosis at the synapse. The scaffolding protein LIN-10/Mint-1 also regulates GLR-1 abundance in the nerve cord. CDK-5 phosphorylates LIN-10/Mint-1 in vitro and bidirectionally regulates the abundance of LIN-10/Mint-1 in the ventral cord. We propose that CDK-5 promotes the anterograde trafficking of GLR-1 and that phosphorylation of LIN-10 may play a role in this process.


1981 ◽  
Vol 84 (1) ◽  
pp. 193-205 ◽  
Author(s):  
Randall Cassada ◽  
Edoardo Isnenghi ◽  
Marilyn Culotti ◽  
Gunter von Ehrenstein

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