Cloning of a new kinesin-related gene located at the centromeric end of the human MHC region

Andõ, Akira; Kikuti, Yara Yukie; Kawata, H.; Okamoto, Naoaki; Imai, Takashi; Eki, Toshihiko; Yokoyama, Kazushige; Soeda, Eiichi; Ikemura, Toshimichi; Abe, Kuniya; Inoko, Hidetoshi

doi:10.1007/bf00241260

Cited by 42 publications

(32 citation statements)

References 25 publications

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“…In line with the distances obtained by FISH, the detection of these fragments positioned HTCTEX-7 proximal to HKE3 and within 130 kb of it. The human homolog of Tctex-7 (HTCTEX-7) was identified as HSET by (Ando et al 1994), and our data are in full agreement with the position given in their paper. …”

supporting

confidence: 91%

Physical Map of Human 6p21.2–6p21.3: Region Flanking the Centromeric End of the Major Histocompatibility Complex

Tripodis¹,

Mason²,

Humphray³

et al. 1998

Genome Res.

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We have physically mapped and cloned a 2.5-Mb chromosomal segment flanking the centromeric end of the major histocompatibility complex (MHC). We characterized in detail 27 YACs, 144 cosmids, 51 PACs, and 5 BACs, which will facilitate the complete genomic sequencing of this region of chromosome 6. The contig contains the genes encoding CSBP, p21, HSU09564 serine kinase, ZNF76, TCP-11, RPS10, HMGI(Y), BAK, and the human homolog of Tctex-7 (HSET). The GLO1 gene was mapped further centromeric in the 6p21.2-6p21.1 region toward TCTE-1. The gene order of the GLO1-HMGI(Y) segment in respect to the centromere is similar to the gene order in the mouse t-chromosome distal inversion, indicating that there is conservation in gene content but not gene order between humans and mice in this region. The close linkage of the BAK and CSBP genes to the MHC is of interest because of their possible involvement in autoimmune disease.The 2.5-Mb chromosomal segment flanking the centromeric end of the major histocompatibility complex (MHC) spans the boundary of the 6p21.2 (Giemsa dark) and 6p21.3 (Giemsa light) bands. This segment is of interest because of the association of the MHC with diseases, particularly of autoimmune etiology and the synteny to the mouse tcomplex distal inversion on chromosome 17 (Hamvas et al. 1996). The conservation between the 4-Mb human MHC and the mouse H2 complex is well documented (Hanson and Trowsdale 1991;Amadou et al. 1995), but for the region centromeric to the MHC, it is not well established.The mouse t-complex is an intensively studied region containing genes, which, when mutated or rearranged, cause a number of effects including embryonic lethality, male sterility, recombination suppression, and transmission ratio distortion (Silver 1993b;Foreijt et al. 1994). A part of this complex, within the distal inversion extending from the mouse Hmgi(y) gene to the H2-K region, contains a number of testis-expressed genes (Abe et al. 1988;Yeom et al. 1992). Testis-expressed sequences have been previously identified centromeric to the MHC (Ragoussis et al. 1992).In humans, this region harbors a gene involved in retinitis pigmentosa (ArP14) (Shugart et al. 1995) whereas chromosomal rearrangements with breakpoints within the region are associated with neoplasia (Johansson et al. 1993;Nilbert et al. 1995;Xiao et al. 1997).To investigate the relationship of this human segment to the mouse t-complex distal inversion, we have assembled YAC and bacterial clone contigs and mapped sequences with known homology between mice and humans. We screened a variety of genomic libraries in different cloning vectors to obtain clones, and we used both fingerprinting-and hybridization-based approaches to construct contigs. The resulting contigs have enabled the construction of transcript maps and are a first step toward construction of sequence-ready bacterial clone contigs. GENOME RESEARCH 631Cold Spring Harbor Laboratory Press on May 12, 2018 -Published by genome.cshlp.org Downloaded from RESULTS Construction of a YAC ContigAs a...

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supporting

confidence: 91%

Physical Map of Human 6p21.2–6p21.3: Region Flanking the Centromeric End of the Major Histocompatibility Complex

Tripodis¹,

Mason²,

Humphray³

et al. 1998

Genome Res.

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“…ID represents identical amino acid residues, and POS represents a positive change in the residue. KLP-3 has 31% ID and 42% POS with Arabidopsis AtKCBP (Reddy, et al, 1996), 36% ID and 66.5% POS with S. cerevisiae nuclear fusion protein Kar3 (Meluh & Rose, 1990), 27.5% ID and 50% POS with Drosophila meiotic and early mitotic chromosome segregation-related protein NCD , 36% ID and 60% POS with A. thaliana kinesin-related protein KatC (Mitsui et al, 1994), 31% ID and 59% POS with A. nidulans kinesin-related protein KLPA (O'Connell et al, 1993) and 25.6% ID and 46% POS with human kinesin-related protein HSET (Ando et al, 1994). Methods: protein homology search and secondary structure predictions: the overall homology was deduced using the BLAST program (Altschul et al, 1990).…”

Section: Northern Blot Analysis Of the Klp-3 Genementioning

confidence: 98%

“…Primary structure and homology of the KLP-3 kinesin Figure 4 shows the motor domain comparison of the KLP-3 kinesin with the yeast S. cerevisiae nuclear fusion protein Kar3 (Meluh & Rose, 1990;Roof et al, 1992) Drosophila meiotic and early mitotic chromosome segregation protein NCD Walker et al, 1990), Arabidopsis thaliana kinesin-related protein KatC (Mitsui et al, 1994), Aspergillus nidulans kinesin-related protein KLPA (O'Connell et al, 1993) and the human kinesin-related protein, also known as HSET (Ando et al, 1994). In addition to the highly signi®cant motor domain homologies, KLP-3 also shows homologies with the Kar3 and ncd kinesins in the non-motor region (data not shown).…”

Section: *Corresponding Authormentioning

confidence: 99%

Molecular cloning and expression of the Caenorhabditis elegans klp-3, an ortholog of C terminus motor kinesins kar3 and ncd

Khan

Gogonea

Siddiqui

et al. 1997

Journal of Molecular Biology

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“…Family members include protein isoforms from Drosophila (Ncd) (Walker et al, 1990;McDonald et al, 1990), hamster (CHO2) (Kuriyama et al, 1995;Matuliene et al, 1999), Xenopus (XCTK2) (Walczak et al, 1997), human (HSET) (Ando et al, 1994;Mountain et al, 1999), mouse (KIFC5A) (Navolanic and Sperry, 2000;Zhang and Sperry, 2004), and others. Although there are differences between species, Kinesin-14 motors, in general, localise to the centrosomes at spindle poles and, through their minus-end motility and ability to bundle MTs, are thought to be important for the formation of focused asters, the establishment of spindle bipolarity and the maintenance of spindle integrity (reviewed by Ovechkina and Wordeman, 2003).…”

Section: Introductionmentioning

confidence: 99%

Motor protein KIFC5A interacts with Nubp1 and Nubp2, and is implicated in the regulation of centrosome duplication

Christodoulou

Lederer

Surrey

et al. 2006

Journal of Cell Science

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Inhibition of motor protein activity has been linked with defects in the formation of poles in the spindle of dividing cells. However, the molecular mechanisms underlying the functional relationship between motor activity and centrosome dynamics have remained uncharacterised. Here, we characterise KIFC5A, a mouse kinesin-like protein that is highly expressed in dividing cells and tissues, and is subject to developmental and cell-type-specific regulation. KIFC5A is a minus-end-directed, microtubule-dependent motor that produces velocities of up to 1.26 μm minute-1 in gliding assays and possesses microtubule bundling activity. It is nuclear in interphase, localises to the centre of the two microtubule asters at the beginning of mitosis, and to spindle microtubules in later mitotic phases. Overexpression of KIFC5A in mouse cells causes the formation of aberrant, non-separated microtubule asters and mitotic arrest in a prometaphase-like state. KIFC5A knockdown partly rescues the phenotype caused by inhibition of plus-end-directed motor Eg5 by monastrol on the mitotic spindle, indicating that it is involved in the balance of forces determining bipolar spindle assembly and integrity. Silencing of KIFC5A also results in centrosome amplification detectable throughout the cell cycle. Supernumerary centrosomes arise primarily as a result of reduplication and partly as a result of cytokinesis defects. They contain duplicated centrioles and have the ability to organise microtubule asters, resulting in the formation of multipolar spindles. We show that KIFC5A interacts with nucleotide-binding proteins 1 and 2 (Nubp1 and Nubp2), which have extensive sequence similarity to prokaryotic division-site-determining protein MinD. Nubp1 and Nubp2 also interact with each other. Knockdown of Nubp1 or double knockdown of Nubp1 and Nubp2 (Nubp1&Nubp2) both phenocopy the KIFC5A silencing effect. These results implicate KIFC5A and the Nubp proteins in a common regulatory pathway involved in the control of centrosome duplication in mammalian cells.

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Cloning of a new kinesin-related gene located at the centromeric end of the human MHC region

Cited by 42 publications

References 25 publications

Physical Map of Human 6p21.2–6p21.3: Region Flanking the Centromeric End of the Major Histocompatibility Complex

Physical Map of Human 6p21.2–6p21.3: Region Flanking the Centromeric End of the Major Histocompatibility Complex

Molecular cloning and expression of the Caenorhabditis elegans klp-3, an ortholog of C terminus motor kinesins kar3 and ncd

Motor protein KIFC5A interacts with Nubp1 and Nubp2, and is implicated in the regulation of centrosome duplication

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