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1 susceptible phenotypes, were pooled (bulked segregant).
2 icrog, and 27.9%, respectively, for isogenic segregants.
3 tance (ApR); recombination generates Lac-ApS segregants.
4 t carries it by killing plasmid-free (cured) segregants.
5 t for a group of genetically different yeast segregants.
6 nctions intracellularly to kill plasmid-free segregants.
7 mapping traits in yeast by genotyping pooled segregants.
8 on contained in tetrads as opposed to single segregants.
9 red on marker D6S1045 at 6q14.3-q15, in 6/19 segregants.
10 production of respiratory-deficient (petite) segregants.
11 r was monitored by selection for TK-positive segregants.
17 nicle1 (spp1) phenotype, we performed bulked segregant analysis and deep sequencing to fine map it to
18 sly applied to Chlamydomonas, such as bulked segregant analysis and marker duplexing, are being imple
21 loral mutant of Mimulus lewisii through bulk segregant analysis and transgenic experiments and identi
22 duced mutant of Mimulus lewisii through bulk segregant analysis and transgenic experiments, we have i
25 t the power of sequencing combined with bulk segregant analysis can also be applied to a nongenetical
26 he applicability of this map, we used bulked segregant analysis followed by interval mapping to locat
29 a tetraploid intermediate, followed by bulk segregant analysis in conjunction with high-throughput s
31 ponsible, we performed flow sorting and bulk segregant analysis of 25 proteins, finding a median of f
37 fragment length polymorphism (AFLP) and bulk segregant analysis were used to map the Def-1 gene to a
38 We genetically mapped the mutations by bulk segregant analysis with high-density oligonucleotide arr
39 trate a new method, microarray-assisted bulk segregant analysis, for mapping traits in yeast by genot
40 idely used mapping techniques like F(2) bulk-segregant analysis, our method produces near-isogenic li
44 Using our first-pass marker panel in bulked-segregant analysis, we were able to identify the genetic
53 olymorphisms at an error rate close to 3% in segregants and at an error rate of 7% in diploid strains
54 by crossing those strains, phenotyping 1500 segregants, and genotyping of high-survival segregants b
55 encodes Doc, a toxin that kills plasmid-free segregants, and Phd, an unstable antidote that neutraliz
58 1-HSV-2 hybrid tk sequences gave rise to tk+ segregants at an average rate of 10(-8) events per cell
59 ations of 10-100 million haploid and diploid segregants by crossing two budding yeast strains of diff
60 segregants, and genotyping of high-survival segregants by hybridization of bulk and single segregant
61 (20%) of these giving rise to transformation segregants containing exclusively the initially nonselec
66 (e) breast cancer data, as well as (f) yeast segregant data to validate the ability of the proposed m
67 ome capture data from bulked early flowering segregants derived from a backcross of the Bowman(eam5)
68 -type (WT; non-mutagenized) genotype, and F2 segregants displaying the same phenotype are subsequentl
70 were then analyzed for linkage using meiotic segregants; four linkage groups were identified in chrom
73 rallel genotype and gene expression data for segregants from a cross between two strains of the yeast
75 ces systematically, we treated 104 genotyped segregants from a cross between two yeast strains with a
76 ated the LIR, as compared to 3% of the tk(+) segregants from LDR cell lines, corresponding to a >20-f
77 i-complementation mutants and transgene-null segregants from RNAi suppression lines to sub-compartmen
79 By sequencing pooled DNA from millions of segregants grown under heat stress, we further identifie
80 on with next-generation sequencing on bulked segregants in the same accession using sequence polymorp
81 r 'cloning by sequencing': one based on bulk segregant linkage (BSFseq) and one based on homozygosity
83 We then developed a population-level bulk segregant mapping method, based on high-throughput genom
85 sis of the introduced chromosome in immortal segregants narrowed the candidate interval to 2.7 Mb spa
86 sequencing in pheromone-treated cells of 43 segregants of a cross between two highly diverged yeast
88 number (one to two copies) in some of the F2 segregants, perhaps resulting from the clustering of PCP
90 analysis of PMN responses to O3 exposure in segregant populations derived from inflammation-prone (s
91 fected with the various substrates and tk(+) segregants produced via intrachromosomal recombination w
93 chromosome complement of individual plants (segregants) ranged from 36 to 42, with a bias toward the
98 formed seed compared with 10.9%TFA in a null segregant seed and 53.2%TFA in the current best source o
101 restored in later generations, even in those segregants that inherited the corresponding parental rDN
102 n and methylation are not heritable: meiotic segregants that lack Ufo1 revert to the normal P1-wr exp
108 quency of disease in the B lymphocyte intact segregants was equivalent to that of standard NOD mice i
109 1c ORF was made in a diploid strain, and the segregants were plated onto sterol supplemented media un
111 cated near the ZEP/ABA1 gene, but the bulked segregant whole genome sequencing approach more efficien
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