Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Expression quantitative trait locus”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources

A genetic and genomic analysis identifies a cluster of genes associated with hematopoietic cell turnover.

Hematopoietic stem cells from different strains of mice vary widely with respect to their cell cycle activity. In the present study we used complementary genetic and genomic approaches to identify molecular pathways affecting this complex trait. We identified a major quantitative trait locus (QTL) associated with variation in cell proliferation in C57BL/6 and DBA/2 mice to a 10 centimorgan (cM) region on chromosome 11. A congenic mouse model confirmed that a genomic interval on chromosome 11 in isolation confers the proliferation phenotype. To detect candidate genes we performed subtractive hybridizations and gene arrays using cDNA from highly enriched stem cells from parental strains. Intriguingly, a disproportionate number of differentially expressed genes mapped to chromosome 11 and, more specifically, these transcripts occurred in 3 distinct clusters. The largest cluster colocalized exactly with the cell cycling QTL. Such clustering suggested the involvement of genetic variation that affects higher-order chromosomal organization. This hypothesis was reinforced by the fact that differentially expressed genes mapped to recombination "coldspots," as a consequence of which clustered genes are collectively inherited. These findings suggest the functional interdependence of these closely linked genes. Our data are consistent with the hypothesis that this isolated cell cycle QTL does not result from a mutation in a single gene but rather is a consequence of variable expression of a collection of highly linked genes.

Animals↗

Spontaneously occurring mutations in the cyclobutane pyrimidine dimer photolyase gene cause different sensitivities to ultraviolet-B in rice.

Sensitivity to ultraviolet-B (UVB) radiation (280-320 nm) varies widely among rice cultivars. We previously indicated that UV-resistant rice cultivars are better able to repair cyclobutane pyrimidine dimers (CPDs) through photorepair than are UV-sensitive cultivars. In this paper, we report that UVB sensitivity in rice, in part, is the result of defective CPD photolyase alleles. Surjamkhi (indica) exhibited greater sensitivity to UVB radiation and was more deficient in CPD photorepair ability compared with UV-resistant Sasanishiki (japonica). The deficiency in CPD photorepair in Surjamkhi resulted from changes in two nucleotides at positions 377 and 888 in the photolyase gene, causing alterations of two deduced amino acids at positions 126 and 296 in the photolyase enzyme. A linkage analysis in populations derived from Surjamkhi and Sasanishiki showed that UVB sensitivity is a quantitative inherited trait and that the CPD photolyase locus is tightly linked with a quantitative trait locus that explains a major portion of the genetic variation for this trait. These results suggest that spontaneously occurring mutations in the CPD photolyase gene cause different degrees of sensitivity to UVB in rice, and that the resistance of rice to UVB radiation could be increased by increasing the photolyase function through conventional breeding or bioengineering.

Amino Acid Sequence↗

Chromosomal mapping of a major quantitative trait locus regulating compensatory renal growth in the rat.

Despite extensive research conducted over the past century, the mechanisms of compensatory renal growth (CRG) remain a mystery. Insight into the mechanisms that regulate CRG might be gained by identifying genetic factors that influence this complex phenotype. In a large set of recombinant inbred strains derived from the spontaneously hypertensive rat and the Brown Norway rat, a genome scan for quantitative trait loci (QTL) that regulate CRG was performed. The CRG score was expressed as a ratio of the weight of the remnant right kidney at 8 wk of age to the weight of the left kidney at 5 wk of age, both adjusted for body weight. QTL mapping was performed using Map Manager QT and the strain distribution patterns of more than 600 genetic markers. It was found that CRG after unilateral nephrectomy is a multifactorially determined trait with a substantial genetic component. The heritability of CRG approached 40%. Genome wide scan analysis revealed significant evidence of linkage to a region of rat chromosome 4 designated Crg 1 that accounted for more than 50% of the additive genetic variance of CRG in the recombinant inbred strains. The detection of a major QTL influencing CRG in the rat should provide new opportunities for identifying mechanisms that regulate this historically enigmatic phenomenon and may also have implications for research on the pathogenesis of end-stage kidney disease.

Adaptation, Physiological↗

Positional candidate gene selection from livestock EST databases using Gene Ontology.

MOTIVATION: The number of expressed sequence tags (ESTs) in GenBank has now surpassed 200,000 for cattle and 100,000 for swine. The Institute of Genome Research (TIGR) has organized these sequences into approximately 60,000 non-redundant consensus sequences (identified by TIGR Gene Indices) for cattle and 40,000 for swine. Anonymous ESTs are of limited value unless they are connected to function. Functional information is difficult to manage electronically because of heterogeneity of meaning and form among databases. The Gene Ontology (GO) Consortium has produced ontologies for gene function with consistent meaning and form across species. Linking livestock EST to gene function through similarity with sequences from other annotation-rich mammals could accelerate: (1) the discovery of positional candidate genes underlying a livestock quantitative trait locus (QTL) and (2) comparative mapping between livestock and other mammals (e.g. humans, mouse and rat). We initiated this investigation to determine if incorporation of the GO into the annotation process could accelerate livestock positional candidate gene discovery. RESULTS: We have associated livestock ESTs with GO nodes through sequence similarity to the NCBI Reference Sequences (RefSeq). Positional candidate genes are identified within minutes that otherwise required days. The schema described here accommodates queries that return GO nodes from terms familiar to biologists, such as gene name, alternate/alias symbol, and OMIM phenotype. AVAILABILITY: Scripts and schema are available on request from the authors.

Animals↗

Molecular mapping of capsaicinoid biosynthesis genes and quantitative trait loci analysis for capsaicinoid content in Capsicum.

Quantitative variation in the accumulation of two major capsaicinoids responsible for pungency in the fruit of chile peppers, capsaicin and dihydrocapsaicin, was analyzed in a cross between the non-pungent Capsicum annuum parent cv. Maor and a pungent Capsicum frutescens parent, accession BG 2816. In order to identify quantitative trait loci (QTLs) for capsaicinoid content, we employed the bulked segregant analysis method and screened bulked DNA from F2 individuals at the extremes of the distribution of capsaicinoid content with RAPD primers. Screening with 400 primers allowed the identification of three loci that were polymorphic between the bulks. These RAPD markers were converted to SCARs and subsequently mapped with additional RFLP markers to chromosome 7 of pepper. QTL interval analysis for individual and total capsaicinoid content identified a major QTL, termed cap, which explained 34-38% of the phenotypic variation for this trait in two growing environments. For all measurements, the allele of the pungent parent BG 2816 at cap contributed to the increased level of pungency. To determine whether known structural genes in the pathway could define a candidate for this QTL, 12 clones obtained from differentially expressed transcripts from placental tissue in pungent peppers were also mapped. None of them had a significant effect on this trait, nor did the allelic state at the locus C, the on/off switch for pungency in pepper, located on chromosome 2. The identity of cap and its effect on capsaicin content in other backgrounds will be addressed in future studies.

Alleles↗

SUG2 controls grain size and weight by influencing GS2 transcription level in rice.

Grain size is a critical yield determinant and a complex quantitative trait in rice. The major quantitative trait locus GS2, which encodes the transcriptional regulator OsGRF4, has been characterized as a key controller of grain size and grain weight in rice. Building upon existing germplasm resources, exploring the upstream and downstream genes of known grain size regulators is an effective approach to gradually refine and expand the molecular regulatory network underlying grain size. Here, we report that a suppressor of the gain-of-function allele GS2AA, SUG2, which encodes an importin β nuclear transport protein. Phenotypic characterization reveals that the sug2 GS2AA mutant exhibits small grains by inhibiting cell expansion in the spikelet hull. Protein interaction analyses demonstrate that SUG2 physically interacts with GS2 both in vivo and in vitro, and the SUG2A mutation reduces SUG2 expression levels and inhibits GS2 transcriptional activation activity, resulting in decreased GS2 expression levels and GS2 protein abundance in sug2 GS2AA. Genetic analyses indicate that SUG2 and GS2 may be partially involved in a common pathway regulating grain size and weight in rice. These findings elucidate the grain size regulatory relationship between SUG2 and GS2 and provide novel insights into the precision breeding of yield optimization in rice.

Oryza↗

Multiple locus linkage analysis of genomewide expression in yeast.

With the ability to measure thousands of related phenotypes from a single biological sample, it is now feasible to genetically dissect systems-level biological phenomena. The genetics of transcriptional regulation and protein abundance are likely to be complex, meaning that genetic variation at multiple loci will influence these phenotypes. Several recent studies have investigated the role of genetic variation in transcription by applying traditional linkage analysis methods to genomewide expression data, where each gene expression level was treated as a quantitative trait and analyzed separately from one another. Here, we develop a new, computationally efficient method for simultaneously mapping multiple gene expression quantitative trait loci that directly uses all of the available data. Information shared across gene expression traits is captured in a way that makes minimal assumptions about the statistical properties of the data. The method produces easy-to-interpret measures of statistical significance for both individual loci and the overall joint significance of multiple loci selected for a given expression trait. We apply the new method to a cross between two strains of the budding yeast Saccharomyces cerevisiae, and estimate that at least 37% of all gene expression traits show two simultaneous linkages, where we have allowed for epistatic interactions. Pairs of jointly linking quantitative trait loci are identified with high confidence for 170 gene expression traits, where it is expected that both loci are true positives for at least 153 traits. In addition, we are able to show that epistatic interactions contribute to gene expression variation for at least 14% of all traits. We compare the proposed approach to an exhaustive two-dimensional scan over all pairs of loci. Surprisingly, we demonstrate that an exhaustive two-dimensional scan is less powerful than the sequential search used here. In addition, we show that a two-dimensional scan does not truly allow one to test for simultaneous linkage, and the statistical significance measured from this existing method cannot be interpreted among many traits.

Chromosome Mapping↗

Research on the genetic variations of a1-fucosytransferase (FUT1) gene in 26 pig breeds.

Enterotoxigenic Escherichia coli F18(ECF18) is a main pathogen that causes edema disease and post-weaning diarrhoea in piglets, and al-fucosytransferase (FUT1) gene has been identified as a candidate gene for controlling the expression of the receptor for ECF18 bacteria. The genetic variations at position 307 nucleotide in open reading frame of FUT1 gene in 26 pig breeds (total 1458 individuals) from 5 western commercial pig breeds and 21 Chinese native pig breeds were investigated by PCR-RFLP. The results showed that the genetic polymorphisms of the FUT1 locus were only detected in 5 western pig breeds and the Chinese Lingao pig breed, 5 western pig breeds possessed 3 different genotypes, and Lingao pig breed had two susceptible genotypes GG and AG, while all the other 20 Chinese native pig breeds only presented the susceptible genotype GG. The results indicated that if M307G-A point mutation in the coding region of FUT1 gene was the key factor determining the expression of the ECF18 receptor, most of Chinese native pig breeds were absent of the genetic background on the resistance to ECF18 bacteria. In this case, it was inferred that the resistance gene to ECF18 might be originated from western pig breeds. In addition, it is of great importance for the conservation of Lingao pig breed as it is the only found Chinese native pig breed possessing resistance M307A allele in FUT1 gene. Generally, compared with exotic pig breeds, Chinese native pig breeds have stronger resistance to edema disease and post-weaning diarrhoea in piglets. The results suggested that further study should be done to identify and characterize putative QTL (quantitative trait locus) or/and the functional gene responsible for the resistance to ECF18 in Chinese native pig breeds.

Alleles↗

Estimation of quantitative trait loci parameters for milk production traits in German Holstein dairy cattle population.

The main objective of this study was to estimate the proportion of total genetic variance attributed to a quantitative trait locus (QTL) on Bos taurus autosome 6 (BTA6) for milk production traits in the German Holstein dairy cattle population. The analyzed chromosomal region on BTA6 spanned approximately 70 cM, and contained 6 microsatellite markers. Milk production data were obtained from routine genetic evaluation for 4500 genotyped German Holstein bulls. Technical aspects related to the estimation of model parameters for a large data set from routine genotype recording were outlined. A fixed QTL model and a random QTL model were introduced to incorporate marker information into parameter estimation and genetic evaluation. Estimated QTL variances, expressed as the ratio of QTL to polygenic variances, were 0.04, 0.03, and 0.07 for milk yield; 0.06, 0.08, and 0.14 for fat yield; and 0.04, 0.04, and 0.11 for protein yield, in the first 3 parities, respectively. The estimated QTL positions, expressed as distances from the leftmost marker DIK82, were 18, 31, and 17 cM for milk yield; 25, 17, and 9 cM for fat yield; and 16, 30, and 17 cM for protein yield in the 3 respective parities. Because the data for the parameter estimation well represented the current population of active German Holstein bulls, the QTL parameter estimates have been used in routine marker-assisted genetic evaluation for German Holsteins.

Analysis of Variance↗

Quantitative trait locus analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels in the (SM/J x A/J)F2 mice.

Quantitative trait locus (QTL) analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels at 10 weeks of age was performed in 321 F2 offspring from SM/J and A/J mice. Interval mapping revealed a total of 22 suggestive QTLs affecting the four traits: two insulin QTLs on Chromosomes (Chrs) 6 and 8; six triglyceride QTLs on Chrs 4, 8, 9, 11, 12 and 19; six total-cholesterol QTLs on Chrs 1, 3, 4, 14, 17 and 19; and eight phospholipid QTLs on Chrs 2, 3, 4, 6, 8, 10 and 19. Gender influenced the expression of eight of the suggestive QTLs. The total-cholesterol QTLs on Chrs 4, 14 and 17, the triglyceride QTL on Chr 9 and the phospholipid QTL on Chr 4 were specific to females. The phospholipid QTLs on Chrs 2 and 6 and the insulin QTL on Chr 8 were specific to males. In addition, common QTLs involved in the regulation of some of the traits were identified. The female-specific QTL on Chr 4 appeared to be involved in the regulation of total cholesterol and phospholipid levels. The QTL on Chr 8 affected insulin and phospholipid levels, whereas the Chr 19 QTL was common to the three lipid parameters.

Animals↗

Mapping of genes expressed in Fusarium graminearum-infected heads of wheat cultivar 'Frontana'.

The isolation, physical, and genetic mapping of a group of wheat genes expressed in infected heads of Triticum aestivum 'Frontana' resistant to Fusarium head blight is reported. A cDNA library was built from heads of 'Frontana' through suppressive subtractive hybridization, to enrich for sequences induced by the pathogen Fusarium graminearum during infection. A group of 1794 clones was screened by dot blot hybridization for differential gene expression following infection. Twenty of these clones showed a strong difference in intensity of hybridization between infected and mock-inoculated wheat head samples, suggesting that they corresponded to genes induced during infection. The 20 clones were sequenced and used for mapping analysis. We determined a precise chromosomal location for 14 selected clones by using series of chromosome deletion stocks. It was shown that the 14 clones detected 90 fragments with the use of the restriction enzyme EcoRI; 52 bands were assigned to chromosome bins, whereas 38 fragments could not be assigned. The selected clones were also screened for polymorphisms on a 'Wuhan' x 'Maringa' wheat doubled haploid mapping population. One clone, Ta01_02b03, was related to a quantitative trait locus for type II resistance located on chromosome 2AL, as determined with simple sequence repeat markers on another mapping population, but did not map in the same location on our population. Another clone, Ta01_06f04, was identified by BLAST (basic local alignment search tool) search in public databases to code for a novel beta-1,3-glucanase, homologous to a major pathogenesis-related protein. This clone mapped to chromosomal regions on chromosome 3, including 3BL and 3DL, where B glucanase gene clusters are known to exist. Seven other clones, including 1 coding for an ethylene-response element binding protein and 3 for ribosomal proteins, and 4 clones corresponding to proteins with unknown function, were also mapped.

Chromosome Mapping↗

Regulatory variation at glypican-3 underlies a major growth QTL in mice.

The genetic basis of variation in complex traits remains poorly understood, and few genes underlying variation have been identified. Previous work identified a quantitative trait locus (QTL) responsible for much of the response to selection on growth in mice, effecting a change in body mass of approximately 20%. By fine-mapping, we have resolved the location of this QTL to a 660-kb region containing only two genes of known function, Gpc3 and Gpc4, and two other putative genes of unknown function. There are no non-synonymous polymorphisms in any of these genes, indicating that the QTL affects gene regulation. Mice carrying the high-growth QTL allele have approximately 15% lower Gpc3 mRNA expression in kidney and liver, whereas expression differences at Gpc4 are non-significant. Expression profiles of the two other genes within the region are inconsistent with a factor responsible for a general effect on growth. Polymorphisms in the 3' untranslated region of Gpc3 are strong candidates for the causal sequence variation. Gpc3 loss-of-function mutations in humans and mice cause overgrowth and developmental abnormalities. However, no deleterious side-effects were detected in our mice, indicating that genes involved in Mendelian diseases also contribute to complex trait variation. Furthermore, these findings show that small changes in gene expression can have substantial phenotypic effects.

Aging↗

Genetic and molecular analysis of smooth, a quantitative trait locus affecting bristle number in Drosophila melanogaster.

A semi-lethal, sterile allele of the smooth locus (2-91.5), sm3, was discovered in an artificial selection line for low abdominal bristle number that had been started from a P-M dysgenic cross. The fitness effects and extremely low bristle number phenotype of the allele could not be separated by recombination from a P-element insertion at cytological location 56E, and precise excision of the P-element at this site was associated with reversion to wild type. The smooth gene was cloned using the P-element insertion as a tag. The gene encodes a 2.6-kb transcript derived from 10 exons and covers a genomic region of at least 80 kb. The Drosophila smooth gene shares substantial sequence identity with a group of RNA binding proteins, with the closest relationship being to the human heterogeneous nuclear ribonucleoprotein L gene. The smooth gene is by definition an abdominal bristle number quantitative trait locus, but further work is required to discern whether naturally occurring allelic variation at this locus is a source of genetic variation for abdominal bristle number in natural populations.

Abdomen↗

Genetic effects on chromatin accessibility reveal the molecular mechanisms of complex traits in maize.

Cis-regulatory elements (CREs) are critical for modulating gene expression and phenotypic diversity in maize. While genome-wide association study (GWAS) hits and expression quantitative trait loci (eQTLs) are often enriched in CREs, their molecular mechanisms remain poorly understood. Characterizing CREs within accessible chromatin regions (ACRs) offers a powerful approach to link noncoding variants to chromatin structure alterations and phenotypic variation. Here, we generated ATAC-seq profiles from seedling leaves of 214 maize inbred lines, identifying 82 174 consensus ACRs. Notably, 39.55% of these ACRs exhibited significant population-wide chromatin accessibility variation. By mapping chromatin accessibility quantitative trait loci (caQTLs), we discovered 27 004 loci, including 1398 predicted to disrupt transcription factor (TF)-binding sites. Integration with multi-omics data revealed 7405 caACR-target gene pairs and linked 56 caACRs to GWAS signals for 51 agronomic traits, with significant enrichment in flowering-related pathways. Functional candidates such as ZmZIM30 - putatively regulated by caACRs - emerged as key regulators of flowering time. At the fad7 locus associated with linolenic acid content, allelic variants overlapping a caQTL showed differential chromatin accessibility. Our study provides a high-resolution cis-elements of maize leaves, deciphers the genetic basis of chromatin accessibility variation, and bridges noncoding caQTLs to molecular mechanisms underlying GWAS hits.

Zea mays↗

Immunoblot analysis of the antibody response to murine cytomegalovirus in genetically resistant and susceptible mice.

The murine of human cytomegalovirus infection was employed to analyse the kinetics of antibody production to murine cytomegalovirus (MCMV) structural and immediate early (IE) polypeptides following MCMV infection of genetically resistant and susceptible strains of mice. A total of 22 structural and six non-structural. IE proteins were identified. Analysis of immunoblots by densitometry identified four patterns of antibody reactivity to MCMV structural polypeptides during primary and secondary antibody responses over a period of 5 weeks post-infection (p.i.). Firstly, antibodies were strongly reactive with an 83K protein soon after infection, with levels which decreased with time: antibodies to a second group of viral proteins were also recognized soon after infection, but consistent levels of reactivity were maintained. Viral proteins that were recognized beyond day 14 p.i. or following a second MCMV infection formed the third group; the fourth consisted of viral proteins that were detected at variable times p.i. by antisera different mouse strains. The kinetics and intensity of the antibody response to individual viral proteins were influenced by virus dose, time p.i. and by a second MCMV infection. In addition, the genetic constitution of the host influenced the antibody response to MCMV proteins both quantitatively and qualitatively. In particular, sera from mice possessing C57BL but not BALB/c genes detected a 56K Mr viral during seroconversion. Antibody reactivity to this protein was shown to segregate among sera from CXB mice, with a strain distribution pattern which indicated a linkage with the b locus on chromosome 4. Finally, expression of the 56K protein was detected in B10. BR but not BALB/c embryo fibroblasts in vitro, with expression being a dominant trait in (BALB/c x B10.BR) F1 embryo fibroblasts. Thus, host genes may influence the expression of this structural viral protein.

Animals↗

Development of overt proteinuria in the Munich Wistar Frömter rat is suppressed by replacement of chromosome 6 in a consomic rat strain.

In a cross between the Munich Wistar Frömter (MWF) rat and spontaneously hypertensive rats (SHR), a major quantitative trait locus (QTL) was identified on rat chromosome 6 (RNO6) that demonstrated the strongest linkage to albuminuria among several QTL identified. The QTL represented the only locus that is linked to both early-onset albuminuria and increased renal interstitial fibrosis in adult animals. A consomic MWF-6(SHR) strain in which chromosome 6 from SHR was introgressed into the MWF background therefore was generated to test the relevance of this QTL. Phenotype analysis at 8 wk of age revealed that early onset of albuminuria in MWF with a 55-fold elevation of urinary albumin excretion compared with SHR (P < 0.0001) was completely abolished in MWF-6(SHR). Time-course analysis until week 24 demonstrated only a moderate increase of urinary albumin excretion in MWF-6(SHR), whereas MWF reached levels in the nephrotic range (16.6 +/- 3.5 versus 162.6 +/- 16.0 mg/24 h; P < 0.0001). At this age, analysis of glomerulosclerosis, tubulointerstitial damage, renal interstitial fibrosis, and renal collagen III mRNA expression revealed a significant improvement of all parameters in MWF-6(SHR) compared with MWF (P < 0.05). At 32 wk, MWF but not MWF-6(SHR) demonstrated overt proteinuria (354.6 +/- 37.6 versus 48.8 +/- 13.2; P < 0.0001), whereas serum urea, cholesterol, and triglyceride concentrations were lower and creatinine clearance was higher in MWF-6(SHR) compared with MWF (P < 0.05). Therefore, although albuminuria in MWF is determined by a complex interplay of several QTL, our data demonstrate that genetic exchange of one locus on RNO6 leads to marked suppression of early-onset albuminuria and renal damage in MWF.

Albuminuria↗

Linkage between IgE receptor-mediated histamine releasability from basophils and gene marker of chromosome 11q13.

BACKGROUND: The genetics of the regulation of the release of mediators involving the interaction of IgE with cells and their ability to release mediators have not been extensively investigated. With use of the candidate gene approach, it was reported that the gene regulating the beta chain of the high-affinity receptor for IgE is on chromosome 11q13. OBJECTIVE: To determine whether gene(s) in chromosome 11q13 may control the expression of maximal histamine release from basophil to anti-IgE stimuli, linkage analysis between this phenotype and the gene marker of chromosome 11q13 was performed. METHODS: Maximal histamine release to anti-IgE and calcium ionophore A23187 and genotyping chromosome 11q13 with use of microsatellite marker (D11S97) were performed in 56 probands with asthma and 59 of their siblings. The linkage was analyzed by affected sib-pair analysis and the quantitative trait locus approach. RESULTS: Maximal histamine release (mean +/- SE) to anti-IgE and A23187 was 43.3% +/- 3.5% and 30.9 +/- 3.4% in probands and 29.5% +/- 2.6% and 22.2% +/- 2.7 in siblings, respectively. Of 20 sib-pairs with the maximal histamine release to anti-IgE more than 33% (mean plus 1 SD of nonasthmatic controls), 11 (55%) shared 2 D11S97 alleles, 9 (45%) shared 1 allele, and neither sib-pair shared identical alleles, which indicates a significant linkage of maximal histamine to anti-IgE and gene marker of chromosome 11q13 (P =.02). The difference (mean +/- SE) of the maximal histamine release to anti-IgE between each proband and sibling was smaller in sib-pairs with 2 identical alleles than in those with 1 identical allele and with no identical allele (14.1% +/- 2.6% vs 25.8% +/- 3.1% vs 41.0% +/- 4.9%). However, the difference (mean +/- SE) to A23187 between each proband and sibling was not different among the 3 groups (9.7% +/- 1.8% vs 17.9% +/- 3.6% vs 10.4% +/- 4.8%). CONCLUSION: Maximal histamine release from basophils to anti-IgE stimuli was linked to the gene marker of chromosome 11q13.

Adolescent↗

Modifying with mitochondria.

An elegant set of mouse crosses has been used to identify a mitochondrial variant that interacts with a nuclear locus on chromosome 10, Ahl, to modify age-related hearing loss. This discovery sets the stage for the identification of factors that modify expression levels and variability of human hearing impairments.

Age Factors↗