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Results: 4

1.
Fig. 2

Fig. 2. From: Mutability and mutational spectrum of chromosome transmission fidelity genes.

Genomic tiling array analysis of CTF2 and CTF9 alleles. Prediction scores across the TOF1 (a) and SMC3 (b) open reading frames in the composite of four CTF2 and three CTF9 alleles respectively (“s” numbers indicate isolate number). A polymorphism in the strain background (asterisk) is also visible in all CTF2/TOF1 alleles. c, d Summary of sequencing data for TOF1 in 11 CTF2 alleles (c) and for SMC3 in three CTF9 alleles (d). Normal protein sequence is schematized as blue for Tof1p and orange for Smc3p.The amino acid number and identity of each mutation is noted. Three TOF1 frameshift mutations are indicated with additional amino acids schematized in red. SMC3 point mutations are indicated in green

Peter C. Stirling, et al. Chromosoma. 2012 June;121(3):263-275.
2.
Fig. 4

Fig. 4. From: Mutability and mutational spectrum of chromosome transmission fidelity genes.

Possible role of CIN in human tumors. CIN mutations may facilitate the evolutionary process underlying tumorigenesis. This concept is also illustrated for mutator phenotypes in the literature (Stratton et al. 2009; Loeb 2011). From left to right, a cellular mutational pathway is fed by intrinsic and extrinsic factors and can lead to a CIN mutation (blue diamond). CIN creates a mutant population in which oncogenic mutations driving proliferation are more likely to occur (red star). The proliferative phenotype and increased CIN facilitate variation (green star) that can help tumors respond to the environmental challenges (e.g., hypoxia, chemotherapy)

Peter C. Stirling, et al. Chromosoma. 2012 June;121(3):263-275.
3.
Fig. 3

Fig. 3. From: Mutability and mutational spectrum of chromosome transmission fidelity genes.

A network of CIN-associated gene ontology terms. GO terms associated with ≥20 CIN genes were included and then filtered for redundant terms to retain the most genes while simplifying the network. Node size is set to number of genes annotated to a term and edge weight is set to the number of genes overlapping between terms. The figure encompasses >80% of the 692 CIN genes reported (Stirling et al. 2011). Blue node color indicates ≥2 genes from the 13 multimember Ctf complementation groups from Spencer et al. (1990) (CTF1CTF12, CTF18) are annotated to that GO term. Darker blue indicates more genes annotated to that term (i.e., establishment of/mitotic sister chromatid cohesion—12 genes; DNA replication—6 genes; DNA repair, meiosis—4 genes; mitosis—3 genes; chromosome, replication fork protection complex, kinetochore—2 genes)

Peter C. Stirling, et al. Chromosoma. 2012 June;121(3):263-275.
4.
Fig. 1

Fig. 1. From: Mutability and mutational spectrum of chromosome transmission fidelity genes.

Features of the chromosome fragment and Ctf assay. a Schematic of chromosome fragment construction as described in the main text (Spencer et al. 1990). Briefly a plasmid with a unique restriction between Y′ and unique sequences (inverted triangle) is digested and used to transform a haploid strain. In this example, recombination (indicated by large X) of the Y′ element (i) fuses the chromosome fragment plasmid to the telomere on the right arm and coordinate recombination of a unique pericentromeric site (ii) fuses the left arm of the chromosome to the plasmid-telomere moiety to generate the independent chromosome fragment (iii). Diagonal lines indicate large chromosomal distances. b Schematic of the Ctf assay. ade2-101 cells form red colonies (left) which are suppressed to a white color by SUP11 (center). Mutagenesis of a Ctf gene leads to red sectors in a white colony. The colony on the far right is half-sectored. The frequency of half-sectored colonies, which are generated by loss of the CF in the first cell division on the plate, can be used to quantify chromosome loss rates

Peter C. Stirling, et al. Chromosoma. 2012 June;121(3):263-275.

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