Abstract:C-terminal kinesin motor proteins, such as the Drosophila NCD and yeast KAR3, are involved in chromosomal segregation. Previously we have described two orthologs of NCD in Caenorhabditis elegans, KLP-3 and KLP-17, which also participate in chromosome movement. Here we report cDNA cloning of klp-15 and klp-16, and the expression pattern of the genes encoding C-terminal motor kinesins including klp-15 and klp-16. Interestingly KLP-15 and KLP-16 form a unique class of C-terminal kinesins, distinct from the previo… Show more
“…Previous work from other groups had suggested a role for KLP-15/16 in the segregation of meiotic chromosomes, because in addition to embryonic lethality, inhibition of these proteins resulted in phenotypes such as polar body defects, a high incidence of male progeny (which results from non-disjunction of the X chromosome in the oocyte) and multiple female pronuclei in the one-cell stage embryo [ 21 , 23 – 28 ]. However, a careful analysis to determine the causes of these segregation errors had not been reported.…”
Section: Resultsmentioning
confidence: 99%
“…Now, we have identified KLP-15 and KLP-16, members of the conserved kinesin-14 family of minus-end-directed kinesins [ 21 ], as factors required for microtubule bundling and organization during acentriolar spindle assembly in C . elegans oocytes; in the absence of these proteins, spindles are unable to maintain stable microtubule bundles and as a result are severely aberrant at metaphase and early anaphase.…”
In many species, oocyte meiosis is carried out in the absence of centrioles. As a result, microtubule organization, spindle assembly, and chromosome segregation proceed by unique mechanisms. Here, we report insights into the principles underlying this specialized form of cell division, through studies of C. elegans KLP-15 and KLP-16, two highly homologous members of the kinesin-14 family of minus-end-directed kinesins. These proteins localize to the acentriolar oocyte spindle and promote microtubule bundling during spindle assembly; following KLP-15/16 depletion, microtubule bundles form but then collapse into a disorganized array. Surprisingly, despite this defect we found that during anaphase, microtubules are able to reorganize into a bundled array that facilitates chromosome segregation. This phenotype therefore enabled us to identify factors promoting microtubule organization during anaphase, whose contributions are normally undetectable in wild-type worms; we found that SPD-1 (PRC1) bundles microtubules and KLP-18 (kinesin-12) likely sorts those bundles into a functional orientation capable of mediating chromosome segregation. Therefore, our studies have revealed an interplay between distinct mechanisms that together promote spindle formation and chromosome segregation in the absence of structural cues such as centrioles.
“…Previous work from other groups had suggested a role for KLP-15/16 in the segregation of meiotic chromosomes, because in addition to embryonic lethality, inhibition of these proteins resulted in phenotypes such as polar body defects, a high incidence of male progeny (which results from non-disjunction of the X chromosome in the oocyte) and multiple female pronuclei in the one-cell stage embryo [ 21 , 23 – 28 ]. However, a careful analysis to determine the causes of these segregation errors had not been reported.…”
Section: Resultsmentioning
confidence: 99%
“…Now, we have identified KLP-15 and KLP-16, members of the conserved kinesin-14 family of minus-end-directed kinesins [ 21 ], as factors required for microtubule bundling and organization during acentriolar spindle assembly in C . elegans oocytes; in the absence of these proteins, spindles are unable to maintain stable microtubule bundles and as a result are severely aberrant at metaphase and early anaphase.…”
In many species, oocyte meiosis is carried out in the absence of centrioles. As a result, microtubule organization, spindle assembly, and chromosome segregation proceed by unique mechanisms. Here, we report insights into the principles underlying this specialized form of cell division, through studies of C. elegans KLP-15 and KLP-16, two highly homologous members of the kinesin-14 family of minus-end-directed kinesins. These proteins localize to the acentriolar oocyte spindle and promote microtubule bundling during spindle assembly; following KLP-15/16 depletion, microtubule bundles form but then collapse into a disorganized array. Surprisingly, despite this defect we found that during anaphase, microtubules are able to reorganize into a bundled array that facilitates chromosome segregation. This phenotype therefore enabled us to identify factors promoting microtubule organization during anaphase, whose contributions are normally undetectable in wild-type worms; we found that SPD-1 (PRC1) bundles microtubules and KLP-18 (kinesin-12) likely sorts those bundles into a functional orientation capable of mediating chromosome segregation. Therefore, our studies have revealed an interplay between distinct mechanisms that together promote spindle formation and chromosome segregation in the absence of structural cues such as centrioles.
“…The C. elegans klp‐3 gene encodes an ortholog of the retrograde C‐terminal kinesin motors such as NcD (63), and is involved in chromosome movement (18). Following the discovery of CeKLP‐3, three additional C‐terminal kinesins in C. elegans , namely CeKLP‐15, CeKLP‐16, and CeKLP‐17, were described (16,17). The motor domain homologies place the later three kinesins in a proximal yet distinct branch, in the phylogenetic tree (Figure 1) (16,17).…”
Section: Group Vi: Ncd/kar3/klp‐3 the Carboxyl Terminus Motorsmentioning
confidence: 99%
“…UNC‐104 (15); in other studies a systematic search for kinesin orthologs in C. elegans revealed kinesin orthologs and novel kinesins that define special subclasses, unique to C. elegans, e.g. klp‐15, klp‐16, klp‐17 (16,17). I have described the 21 kinesins in C. elegans , and how they fall into the distinct structural and functional groups found in other organisms.…”
mentioning
confidence: 99%
“…I have described the 21 kinesins in C. elegans , and how they fall into the distinct structural and functional groups found in other organisms. The cDNA cloning of the members of kinesin family members from C. elegans using degenerate primers specific for the highly conserved ATP and microtubule binding sites in the motor domain of kinesin has been described (16–18). The function of C. elegans kinesins has been predicted based on structural homology, gene expression data such as the mRNA in situ hybridization (19), and the gene knockout phenotype analysis using the RNA interference assay (20).…”
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