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PubMed2004

Mapping quantitative trait loci that influence blood levels of alkaline phosphatase in MRL/MpJ and SJL/J mice.

To examine the hypothesis that serum alkaline phosphatase (ALP) levels have a heritable component, we analyzed blood from two inbred strains of mice, MRL/MpJ and SJL, which exhibit 90% difference in total serum ALP activity (268+/-26 vs. 140+/-15 U/l, respectively, P<0.001). A genome-wide scan was carried out using 137 polymorphic markers in 518 F2 female mice. Serum ALP activity in the F2 progeny showed a normal distribution with an estimated heritability of 56%. Genome-wide scan for cosegregation of genetic marker data with serum ALP activity revealed three major quantitative trait loci (QTL), one each on chromosomes 2 (LOD score 3.8), chromosome 6 (LOD score 12.0), and chromosome 14 (LOD score 3.7). In addition, there was one suggestive QTL on chromosome 2 (LOD score of 3.3). In aggregate, these QTLs explain 22.5% of variance in serum ALP between these two strains. Serum ALP showed a moderate but significant correlation with body weight adjusted total body bone mineral density (r=0.12, P=0.0108) and periosteal circumference at midshaft tibia (r=0.15, P=0.0006) in F2 mice. The chromosome 6 locus harboring the major serum ALP QTL also contains a major BMD and bone size QTL, identified earlier, between these two strains of mice; in addition, this QTL is also close to the locus that regulates IGF-I levels (LOD score 8-9) in C3HB6 F2 mice. These common QTLs indicate that the observed difference in ALP and BMD or bone size may be regulated by same loci (or genes). Accordingly, the osteoblast cells isolated from femur and tibia of MRL mice showed a significantly higher number of ALP +ve cells/colony and two- to threefold higher ALP activity (P<0.001) as compared to the cells isolated from SJL mice, thus suggesting that differences in serum ALP between MRL and SJL reflect difference in ALP expression from osteoblasts from these strains of mice. These data suggest that serum ALP levels are genetically determined and correlate with cellular mechanisms that differentiate BMD accrual in these two strains of mice. The findings that ALP and BMD traits share the same loci on chromosome 6 suggest a role for genetic determinants of bone formation in overall BMD accretion.

Alkaline Phosphatase↗
PubMed2004

Protein C levels are regulated by a quantitative trait locus on chromosome 16: results from the Genetic Analysis of Idiopathic Thrombophilia (GAIT) Project.

OBJECTIVE: Protein C (PC) is a component of the protein C anticoagulant pathway. PC deficiency is a risk factor associated with venous thromboembolism. As part of the Genetic Analysis of Idiopathic Thrombophilia (GAIT) Project, we conducted a genome-wide linkage scan to localize genes that influence variation in PC plasma levels. METHODS AND RESULTS: PC levels were measured in 398 individuals belonging to 21 Spanish families. A total of 485 DNA microsatellite markers were genotyped to provide a 7.1-cM genetic map. Variance component linkage methods were used to evaluate linkage and to detect quantitative trait loci (QTL). A region on chromosome 16 (16q23), flanked by markers D16S3106 and D16S516, showed strong evidence of linkage with PC levels (LOD=3.69). This region contains 1 positional candidate gene, the NAD(P)H:dehydrogenase quinone 1 (NQO1), involved in vitamin K metabolism. The association of 1 SNP of this gene with PC levels (P=0.005) strongly supports the implication of NQO1 gene in the variability of PC levels. CONCLUSIONS: These results illustrate the application of genomic scans to identify the genetic determinants of quantitative variation in a component of the hemostatic pathways. They provide strong evidence for a locus (QTL) on chromosome 16 that influences PC levels.

Adolescent↗
PubMed1995

Quantitative trait loci associated with the behavioral response of B x D recombinant inbred mice to restraint stress: a preliminary communication.

Quantitative trait loci (QTL) analysis was used to make provisional identification of loci containing genes influencing vulnerability to stress. The effect of restraint stress on open-field activity was measured in C57BL/6J and DBA/2J inbred strains of mice and in 22 B x D recombinant inbred strains of mice. QTL analyses were performed by correlating the behavioral delta scores for each group with the strain distribution pattern of 1300 markers for the B x D mice. A significant association was found between postrestraint rearings during min 5 through 8 in the open field and the Lamb2 marker on chromosome 1 (r = .718, p < .0001). Significant associations at the p < .0001 level were also found between baseline open-field rearings of control mice during min 0 through 5 and the Zp3, Ache, and Mr66-1 markers on chromosome 5, baseline open-field rearings of control mice during min 5 through 8 and the Pmv42 marker on chromosome 15, and open-field rearings of experimental mice during min 0 through 5 and the D11Ncvs61 marker on chromosome 11.

Animals↗
PubMed1996

Quantitative trait loci for ethanol sensitivity in the LS x SS recombinant inbred strains: interval mapping.

We are mapping the genes (quantitative trait loci or QTLs) that are responsible for individual differences in ethanol sensitivity, measured as the duration of loss of righting, reflex (LORR) and blood ethanol concentrations upon recovery of the righting reflex (BEC). The Long-Sleep (LS) and Short-Sleep (SS) selected lines of mice manifest an 18-fold difference in LORR and serve as a rodent model for ethanol sensitivity. The LS x SS recombinant inbred (RI) series, developed from LS and SS lines, are an important resource for QTL mapping of ethanol-related responses. The current report summarizes the initial QTL analysis of LORR and BEC in the LS x SS strains and compares the results of correlational analysis with an interval-mapping approach. The data provide strong evidence for QTLs that influence ethanol sensitivity on mouse chromosomes 1 and 2 and possible QTLs on chromosomes 1, 3, 4, 5, 6, 7, 12, 13, 16, and 18. These results are compared to those from an F2 cross which confirms QTLs on chromosomes 1, 2, 4, and 18.

Alcohol Drinking↗
PubMed1990

Using molecular markers to estimate quantitative trait locus parameters: power and genetic variances for unreplicated and replicated progeny.

Many of the progeny types used to estimate quantitative trait locus (QTL) parameters can be replicated, e.g., recombinant inbred, doubled haploid, and F3 lines. These parameters are estimated using molecular markers or QTL genotypes estimated from molecular markers as independent variables. Experiment designs for replicated progeny are functions of the number of replications per line (r) and the number of replications per QTL genotype (n). The value of n is determined by the size of the progeny population (N), the progeny type, and the number of simultaneously estimated QTL parameters (q - 1). Power for testing hypotheses about means of QTL genotypes is increased by increasing r and n, but the effects of these factors have not been quantified. In this paper, we describe how power is affected by r, n, and other factors. The genetic variance between lines nested in QTL genotypes (sigma 2n:q) is the fraction of the genetic variance between lines (sigma 2n) which is not explained by simultaneously estimated intralocus and interlocus QTL parameters (phi 2Q); thus, sigma 2n:q = sigma 2n - phi 2Q. If sigma 2n:q not equal to 0, then power is not efficiently increased by increasing r and is maximized by maximizing n and using r = 1; however, if sigma 2n:q = 0, then r and n affect power equally and power is efficiently increased by increasing r and is maximized by maximizing N.r. Increasing n efficiently increases power for a wide range of values of sigma 2n:q.sigma 2n:q = 0 when the genetic variance between lines is fully explained by QTL parameters (sigma 2n = phi 2Q).(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗
PubMed1994

The power of interval mapping of quantitative trait loci, using selected sib pairs.

The interval-mapping procedure of Fulker and Cardon for analysis of a quantitative-trait loci (QTL) is extended for application to selected samples of sib pairs. Phenotypic selection of sib pairs, which is known to yield striking increases in power when a single marker is used, provides further increases in power when the interval-mapping approach is used. The greatest benefits of the combined approach are apparent with coarse maps, where QTLs of relatively modest (15%-20%) heritability can be detected with widely spaced markers (40-60 cM apart) in reasonably sized sibling samples. Useful information concerning QTL location is afforded by interval mapping in both selected and unselected samples.

Algorithms↗
PubMed1999

Preweanling sensorial and motor development in laboratory mice: quantitative trait loci mapping.

Chromosomal mapping of genes linked with 19 measures of sensorial, motor, and body weight development were investigated. Chromosomal mapping is the first step towards gene identification. When a genomic region is shown to be linked to a trait, it is possible to select a reduced number of candidate genes that have been previously mapped on this region. The involvement of every gene can be individually tested either by molecular (transgenesis, homologous recombination) or traditional methods (congenicity). Mapping was performed using 389 males and females from two inbred strains of laboratory mice C57BL/6By and NZB/BlNJ, their reciprocal F1s and F2s. Thirty-six Quantitative Trait Loci (QTL) were mapped, 12 reached the 3.13 lod score, being thus considered as confirmed. These QTL were tentatively labeled: Cliff Drop Aversion (Cliff Qtl), Geotaxia (Geot Qtl), Vertical Clinging (VertCling Qtl), Bar Holding with the 4 paws (BH4P Qtl), Age at Eyelid Opening (Aeyo Qtl), Visual Placing (Vispl Qtl), Startle Response (Start Qtl1, Start Qtl2), Body Weight at Day 10 in Males pooled with Females (Bwefmd10 Qtl), and Body Weight at Day 30 in males (Bwemd30 Qtl). For the majority of the developmental measures, the QTL that were mapped contributed little to the phenotypic variance, even when mitochondrial DNA contribution was included: Righting Response (12.7%), Cliff Drop Aversion (10%), Crossed Extensor Response (18.1%), Geotaxia (16.2%), Bar Holding Response for 10 s (12.1%), Bar Holding Response with 4 paws (8.1%), Vertical Clinging (9.3%), Vertical Climbing (5%), Startle Response (21.2%), Eyelid Opening (14.6%), Visual Placing (22%), Body Weight at Day 10 (27%), Body Weight at Day 15 in Females (52.5%), Body Weight at Day 15 in Males (17%), Body Weight at Day 30 in Females (42%), and Body Weight at Day 30 in Males (48%). A factorial analysis of the correlations between the measures of development did not provide evidence of a general factor. A general genetic factor of development was also rejected because few common genetic correlates were discovered for the 19 measures of development (Body Weight at Days 15 and 30 in Females on Chromosome 2, Eyelid Opening and Body Weight at Day 10 on Chromosome 5 and mitochondrial genome for five measures). Co-identification of genes, the function of which were previously known thanks to newly discovered QTL, should help to explain the function of QTL. Present data help to highlight candidate regions including several genes that could be candidates for the QTL function. Large confidence intervals were obtained as usual from the F2 intercrossed population. More stringent methods are suggested for more efficient co-identification.

Animals↗
PubMed2000

Mapping quantitative trait loci that regulate sensitivity and tolerance to quinpirole, a dopamine mimetic selective for D(2)/D(3) receptors.

Acute sensitivity and tolerance to quinpirole (a dopamine mimetic with selectivity for D(2)/D(3) dopamine receptors) were evaluated in the C57BL/6J and DBA/2J inbred strains of mice, 24 of their BXD recombinant inbred strains, and 233 F(2) mice. Baseline locomotor activity, locomotor activity following 0.03 mg/kg quinpirole (and 0. 01 mg/kg in BXD mice), body temperature following 1 mg/kg quinpirole, and hypothermic tolerance following 2 or 3 days of quinpirole administration were evaluated. Quantitative trait locus (QTL) analysis was employed to identify genetic determinants of baseline locomotor activity and five behavioral responses to quinpirole. We examined correlated allelic variation in genetic markers of known chromosomal location with variation in each of these phenotypes. We definitively mapped a QTL on Chromosome (Chr) 9 linked to the D(2) dopamine receptor gene, Drd2, for hypothermic sensitivity to quinpirole, and identify a suggestive QTL in the same chromosomal region for tolerance to quinpirole after repeated treatments. Suggestive QTLs were also identified on Chr 19 for sensitivity and tolerance to quinpirole-induced hypothermia and for baseline locomotor activity; on Chr 15 for locomotor sensitivity to quinpirole; and on Chr 13 and 5 for baseline locomotor activity. Our results indicate that genetic differences in quinpirole sensitivity and tolerance are associated with QTLs near Drd2, and that baseline locomotor activity is associated with a suggestive QTL in proximity to the dopamine transporter gene Dat1. These data suggest that the genes influencing locomotor activity, dopamine mimetic sensitivity, and tolerance do not overlap completely.

Animals↗
PubMed2004

Identification of quantitative trait loci controlling resistance to maize chlorotic dwarf virus.

Ineffective screening methods and low levels of disease resistance have hampered genetic analysis of maize (Zea mays L.) resistance to disease caused by maize chlorotic dwarf virus (MCDV). Progeny from a cross between the highly resistant maize inbred line Oh1VI and the susceptible inbred line Va35 were evaluated for MCDV symptoms after multiple virus inoculations, using the viral vector Graminella nigrifrons. Symptom severity scores from three rating dates were used to calculate area under the disease progress curve (AUDPC) scores for vein banding, leaf twist and tear, and whorl chlorosis. AUDPC scores for the F(2) population indicated that MCDV resistance was quantitatively inherited. Genotypic and phenotypic analyses of 314 F(2) individuals were compared using composite interval mapping (CIM) and analysis of variance. CIM identified two major quantitative trait loci (QTL) on chromosomes 3 and 10 and two minor QTL on chromosomes 4 and 6. Resistance was additive, with alleles from Oh1VI at the loci on chromosomes 3 and 10 contributing equally to resistance.

Alleles↗
PubMed2006

Identifying loci under selection across contrasting environments in Avena barbata using quantitative trait locus mapping.

We constructed recombinant inbred lines of a cross between naturally occurring ecotypes of Avena barbata (Pott ex Link), Poaceae, associated with contrasting moisture environments. These lines were assessed for fitness in common garden reciprocal transplant experiments in two contrasting field sites in each of two years, as well as a novel, benign greenhouse environment. An AFLP (amplified fragment length polymorphism) linkage map of 129 markers spanned 644 cM in 19 linkage groups, which is smaller, with more linkage groups, than expected. Therefore parts of the A. barbata genome remain unmapped, possibly because they lack variation between the ecotypes. Nevertheless, we identified QTL (quantitative trait loci) under selection in both native environments and in the greenhouse. Across years at the same site, the same loci remain under selection, for the same alleles. Across sites, an overlapping set of loci are under selection with either (i) the same alleles favoured at both sites or (ii) loci under selection at one site and neutral at the other. QTL under selection in the greenhouse were generally unlinked to those under selection in the field because selection acted on a different trait. We found little evidence that selection favours alternate alleles in alternate environments, which would be necessary if genotype by environment interaction were to maintain genetic variation in A. barbata. Additive effect QTL were best able to explain the genetic variation among recombinant inbred lines for the greenhouse environment where heritability was highest, and past selection had not eliminated variation.

Chromosome Mapping↗
PubMed2002

Quantitative trait locus mapping of susceptibilities to butylated hydroxytoluene-induced lung tumor promotion and pulmonary inflammation in CXB mice.

We have reported previously [Bauer,A.K. et al. (2001) Exp. Lung Res., 27, 197-216] that the 13 CXB recombinant inbred mouse strains derived from BALB/cByJ and C57BL/6J progenitors vary in their responsiveness to both lung tumor promotion and pulmonary inflammation induced by chronic administration of butylated hydroxytoluene (BHT). Herein we have applied these data, along with markers known to be polymorphic among these strains, to conduct linkage analysis of these susceptibilities. This enabled us to assign provisional quantitative trait loci (QTL) that govern these strain variations in susceptibility as a genetic approach to assessing the influence of inflammation on tumorigenesis. A Chr 15 (39.1-55.6 cM) QTL regulated susceptibility to two-stage carcinogenesis, a protocol in which chronic BHT exposure followed a single urethane injection; a similar QTL on Chr 15 (46.7-61.7 cM) influenced BHT induction of cyclooxygenase-2 (COX-2) expression. A Chr 18 (37-41 cM) QTL modulated both the number of lung tumors induced by 3-methylcholanthrene (MCA) injection with subsequent treatment with BHT as well as BHT-induced ingress of macrophages into airways. Other chromosomal sites that affected either the degree of BHT-elicited macrophage infiltration, Chr 9 (48-61 cM), or COX-2 induction, Chr 10 (59-65 cM), were reported to influence susceptibility to lung tumorigenesis in other strains. The fact that common chromosomal locations regulate both inflammation and carcinogenesis suggests a pathogenic role of inflammatory mediators in tumor development that may be exploited for chemoprevention of lung cancer.

Animals↗
PubMed1998

Identification of a quantitative trait locus influencing plasma insulin levels after 70% pancreatectomy using the OLETF rat.

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese-type non-insulin-dependent diabetes mellitus (NIDDM) in humans. The OLETF rat has poor capacity for proliferation of pancreatic beta-cells after partial pancreatectomy, which may be the critical pathogenetic event in NIDDM development. The poor pancreatic beta-cell proliferation in this model is characterized by reduction in beta-cell mass and decrease in insulin content in the remnant pancreas. Our investigation was designed to identify quantitative trait loci (QTLs) responsible for beta-cell mass and plasma insulin levels after partial pancreatectomy by performing a genome-wide scan in an F2 intercross obtained by mating the OLETF and the Fischer-344 (F344) rats. We have identified a suggestive QTL for the plasma insulin levels, near D20Mgh5 on rat chromosome 20, with a maximum lod score of 3.75 which accounts for 20% of the total variance, while no QTLs were detected for beta-cell mass. This chromosome 20 QTL, whose OLETF allele is associated with low plasma insulin levels through acting in an incompletely recessive manner, may affect insulin secretion itself rather than beta-cell proliferation.

Animals↗
PubMed1999

Mapping quantitative trait loci for seizure response to a GABAA receptor inverse agonist in mice.

To define the genetic contributions affecting individual differences in seizure threshold, a beta carboline [methyl-beta-carboline-3-carboxylate (beta-CCM)]-induced model of generalized seizures was genetically dissected in mice. beta-CCM is a GABAA receptor inverse agonist and convulsant. By measuring the latency to generalized seizures after beta-CCM administration to A/J and C57BL6/J mice and their progeny, we estimated a heritability of 0.28 +/- 0.10. A genome wide screen in an F2 population of these parental strains (n = 273) mapped quantitative trait loci (QTLs) on proximal chromosome 7 [logarithm of the likelihood for linkage (LOD) = 3.71] and distal chromosome 10 (LOD = 4.29) for seizure susceptibility, explaining approximately 22 and 25%, respectively, of the genetic variance for this seizure trait. The best fitting logistic regression model suggests that the A/J allele at each locus increases the likelihood of seizures approximately threefold. In a subsequent backcross population (n = 223), we mapped QTLs on distal chromosome 4 (LOD = 2.88) and confirmed the distal chromosome 10 QTLs (LOD = 4.36). In the backcross, the C57BL/6J allele of the chromosome 10 QTL decreases the risk of seizures approximately twofold. These QTLs may ultimately lead to the identification of genes influencing individual differences in seizure threshold in mice and the discovery of novel anticonvulsant agents. The colocalization on distal chromosome 10 of a beta-CCM susceptibility QTL and a QTL for open field ambulation and vertical movement suggests the existence of a single, pleiotropic locus, which we have named Exq1.

Animals↗
PubMed2003

ENU large-scale mutagenesis and quantitative trait linkage (QTL) analysis in mice: novel technologies for searching polygenetic determinants of craniofacial abnormalities.

Discrepancies in size and shape of the jaws are the underlying etiology in many orthodontic and orthognathic surgery patients. Genetic factors combined with environmental interactions have been postulated to play a causal or contributory role in these craniofacial abnormalities. Along with the soon-to-be-available complete human and mouse genomic sequence data, mouse mutants have become a valuable tool in the functional mapping of genes involved in the development of human maxillofacial dysmorphologies. We review two powerful methods in such efforts: N-ethyl-N-nitrosourea (ENU) large-scale mutagenesis and quantitative trait linkage (QTL) analysis. The former aims at producing a plethora of novel variants of particular trait(s), and ultimately mapping the point mutations responsible for the appearance of these new traits. In contrast, the latter applies intensive breeding and mapping techniques to identify multiple loci (and, subsequently, genes) contributing to the phenotypic difference between the tested strains. A prerequisite for either approach to studying variations in the traits of interest is the application of effective mouse cephalometric phenotype analysis and rapid DNA mapping techniques. These approaches will produce a wealth of new data on critical genes that influence the size and shape of the human face.

Alkylating Agents↗
PubMed2001

A chromosome 15 quantitative trait locus controls levels of radiation-induced jejunal crypt cell apoptosis in mice.

Jejunal crypt cells undergo apoptosis in response to ionizing radiation exposure. In mice the number of cells deleted by apoptosis is determined by several factors including the dose of radiation, the time of day the apoptosis level is quantified, and the strain of mouse irradiated. We previously found that the difference in radiation-induced apoptosis levels between C57BL/6J (B6) and C3Hf/Kam (C3H) mice is controlled by multiple genes, and this set of genes is distinct from that controlling thymocyte apoptosis levels in the same strain combination. Here, we report that a new quantitative trait locus on chromosome 15, Rapop5, partly accounts for the murine strain difference in susceptibility to radiation-induced jejunal crypt cell apoptosis. In addition, we show sexual dimorphism in the extent of radiation-induced jejunal crypt cell apoptosis, with female mice having higher levels.

Animals↗
PubMed2003

Quantitative trait loci for susceptibility to tapeworm infection in the red flour beetle.

Parasites have profound effects on host ecology and evolution, and the effects of parasites on host ecology are often influenced by the magnitude of host susceptibility to parasites. Many parasites have complex life cycles that require intermediate hosts for their transmission, but little is known about the genetic basis of the intermediate host's susceptibility to these parasites. This study examined the genetic basis of susceptibility to a tapeworm (Hymenolepis diminuta) in the red flour beetle (Tribolium castaneum) that serves as an intermediate host in its transmission. Quantitative trait loci (QTL) mapping experiments were conducted with two independent segregating populations using amplified fragment length polymorphism (AFLP) markers and randomly amplified polymorphic DNA (RAPD) markers. A total of five QTL that significantly affected beetle susceptibility were identified in the two reciprocal crosses. Two common QTL on linkage groups 3 and 6 were identified in both crosses with similar effects on the phenotype, and three QTL were unique to each cross. In one cross, the three main QTL accounted for 29% of the total phenotypic variance and digenic epistasis explained 39% of the variance. In the second cross, the four main QTL explained 62% of the variance and digenic epistasis accounted for only 5% of the variance. The actions of these QTL were either overdominance or underdominance. Our results suggest that the polygenic nature of beetle susceptibility to the parasites and epistasis are important genetic mechanisms for the maintenance of variation within or among beetle strains in susceptibility to tapeworm infection.

Animals↗
PubMed2001

A quantitative trait locus influencing estrogen levels maps to a region homologous to human chromosome 20.

Estrogen, a steroid hormone, regulates reproduction and has been implicated in several diseases. We performed a genome-wide scan using multipoint linkage analysis implemented in a general pedigree-based variance component approach to identify genes with measurable effects on variation in estrogen levels in baboons. A microsatellite polymorphism, D20S171, located on human chromosome 20q13.11, showed strong evidence of linkage with a LOD score of 3.06 (P = 0.00009). This region contains several potential candidate genes including melanocortin 3 receptor (MC3R), cytochrome P-450 subfamily XXIV (CYP24), and breast carcinoma amplified sequence (BCAS1). This is the first evidence of a quantitative trait locus with a significant effect on estrogen.

Aging↗
PubMed2006

Quantitative trait loci analysis of leaf and plant longevity in Arabidopsis thaliana.

The natural variation in leaf and plant longevity in Arabidopsis thaliana was analysed in a set of 45 ecotypes and 155 recombinant inbred lines derived from a Cape Verde Islands (Cvi) x Landsberg erecta (Ler) cross. Post-bolting longevity was inversely related to time to flowering and rosette leaf number in the set of 45 ecotypes, with Cvi having the longest and Ler the shortest post-bolting longevity. The recombinant inbred line population was tested under low or high soil nutrient levels (LN or HN, respectively). Three quantitative trait loci (QTL), one in chromosome 3 and two in chromosomes 1 and 5, were associated with longevity of the 6th rosette leaf under LN and HN, respectively. Four QTL for post-bolting longevity were found in chromosomes 1, 3, 4, and 5, and two in chromosomes 1 and 5 under LN and HN, respectively. An epistatic interaction affecting post-bolting longevity under LN, but not HN, was detected. Ler and Cvi carry a mix of increasing and decreasing alleles for the QTL affecting longevity of the 6th leaf and post-bolting longevity. Longevity of the 6th rosette leaf was associated with different QTL than post-bolting longevity, and it was affected by different QTL depending on nutrient availability. By contrast, the major QTL affecting post-bolting longevity exerted significant effects irrespective of soil nutrient availability.

Arabidopsis↗