Deletion mapping

Stanczak CM, Chen Z, Zhang YH, Nelson SF, McCabe ERB (2007) Deletion mapping in Xp21 for patients with complex glycerol kinase deficiency using SNP mapping arrays. Hum Mutat 28 235-242... 

Mainville, C.A., Sheehan, K.M., Klaman, L.D., Giorgetti, C.A., Press, J.L., Brodeur, P.H. (1996). Deletional mapping of fifteen mouse VH gene families reveals a common organization for three Igh haplotypes. J. Immunol. 156, 1038-1046. 

Cheng JQ, Jhanwar SC, Klein WM, et al. 1994. pl6 alterations and deletion mapping of 9p21-p22 in malignant mesothelioma. Cancer Res 54 5547-5551. 

Lu YY, Jhanwar SC, Cheng JQ, et al. 1994b. Deletion mapping of the short arm of chromosome 3 in human malignant mesothelioma. Genes Chromosomes Cancer 9 76-80. 

GFP from the jellyfish Aequorea victoria has 238 residues, which form 11 / -sheets arranged in a barrel shape (Fig. 5.2). The barrel is a nearly perfect cylinder with a height of 42 A and a radius of 12 A. The chromophore is located in the middle of the so-called / -barrel and deletion mapping experiments have shown that nearly the entire structure (residues 2-232) is required for chromophore formation and/or fluorescence [18]. 

Fig. 4. Organization of the mouse Igh locus. The order of Vu gene families is based on Igh recombinant mouse strains [27] and deletion mapping studies [Brodeur. unpublished]. Approximate location of genetic cross-overs are designated by X. Distance (molecular and rccombinational) between or within V, gene families are unknown. The map position of the VnJ558 family is tentative (see text).

The arrangement of genes encoded by pOP12 has also been determined by deletion mapping experi-... 

Lewin A., Morimoto R., Rabinowitz M. (1978). Restriction enzyme analysis of mitochondrial DNAs of petite mutants of yeast classification of petites, and deletion mapping of mitochondrial genes. Mol. Gen. Genet. 163 257-275. 

Fig. 1 Three representative cases of wPPIs. Case I a weak protein-protein interaction found in a locally highly crowded manner. Case II a weak domain-domain interaction, exemplified by A-B pair, as part of a tight multi-domain complex. Such weak binary domain-domain interaction may be undetectable by many conventional methods including deletion mapping, yeast-hybrid approach, immunoprecipitation, etc., but become apparent when the tertiary structure of the tight complex is challengingly determined. However, NMR may be able to pick this interaction at early stage of the characterization. Case III a weak protein-protein interaction as a part of multi-protein complex. Similar to II), a weak A-D pair may not be detectable in isolated manner by any conventional techniques except NMR...

Fig. 4. Structural genes araD, araA, and araB. Mutant sites indicated were previously ordered by three-factor reciprocal crosses. The order of a number of these sites, indicated by a heavy vertical line, has been confirmed by deletion mapping. Circled numbers indicate the site of mutations producing CRM. The stars indicate nonsense mutations. The dimensions in the figure do not represent the actual sizes of the gene.

Fig. 5. The regulatory gene, araC. The gene is divided into six sections by the deletions. The numbers above the small vertical line represent the site of C mutants ordered by three-factor reciprocal crosses and are placed at relative distances from one another based on recombination frequencies. (C/0/ to CI9 = 3.65 recombination units.) Other C mutant sites ordered by three-factor reciprocal crosses but without distance measurements are indicated only by a number (42,49,57). The order of several of the C mutant sites was confirmed by mapping with the deletion mutants indicated. mutants C 1-I0, C 60-67) isolated as resistant to o-fucose inhibition were mapped by recombination frequency. The position of mutant site C67, C 2, C4, and C 70 as being within the C gene was verified by deletion mapping. mutants (100 and over) isolated from a dK strain were ordered by deletion mapping. The star represents a nonsense mutation.

Constitutive mutants (C) for the L-arabinose pathway have been isolated from the wild type as mutants resistant to the D-fucose inhibition of growth on mineral L-arabinose D-fucose medium and from D-ribulokinaseless mutants dK ) as double mutants dK O) able to grow on mineral D-arabinose medium (see Sections II,B,1 II,B,2). The former C mutants were mapped by recombination frequencies [6]. With the availability of deletions ending at various positions within the araC gene, it became possible to map the C mutant sites using deletion mapping. All the C mutations isolated as dK C were mapped by this procedure [54] (Fig. 5). 

Of the 22 C mutants, isolated as resistant to D-fucose, 18 mapped between C" mutant sites. C8 and C 70 mapped close to C5. Both failed to give any wild-type recombinants with C5, and based on the number of Ara recombinants assayed, it was estimated that C 8 and 070 are, respectively, less than 0.02 and 0.1 recombination unit away from C5. The position of other mutant sites 067, 02, 04, 070) as being within the C gene was verified by deletion mapping [14]. 

Fromm, M., and Berg, P., 1982, Deletion mapping of DNA regions required for SV40 early region promoter function in vivo, J. Mol. Appl. Gen. 1 457-481. 

Dopf, J. and Horiagon, T.M., Deletion mapping of the Aequorea victoria green fluorescent protein. Gene, 173, 39-44, 1996. 

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