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At least 55 records · Page 3Linked to original sources
PubMed2002

Inducible and endothelial nitric oxide synthase: genetic background affects ovulation in mice.

OBJECTIVE: Inducible nitric oxide synthase (NOS) and endothelial NOS are involved in female reproductive physiology. We sought to investigate the influence of the inducible (Nos2) and endothelial (Nos3) NOS genes as a function of genetic background on ovulatory capacity and early embryonic development in a mouse model. DESIGN: Observational study of genetically altered mice and their response to a superovulation protocol. SETTING: Academic research institution. ANIMALS: Wild-type mice and mice deficient for Nos2 or Nos3 were bred to C57BL/6J and 129/Sv genetic backgrounds. INTERVENTION(S): Superovulation protocol, oocyte culture. MAIN OUTCOME MEASURE(S): Number of oocytes harvested, early embryonic development of zygotes, evaluation of ovarian histology. RESULT(S): The mean number of oocytes was significantly reduced in Nos3 deficient mice on a C57BL/6J background compared with controls. Oocytes deficient for Nos3 on a C57BL/6J background also showed reduced progression to two-cell stage embryos after 24 hours, two-cell stage embryos to blastocyst stage embryos, and survival to 48 hours. Those effects were distinctly absent in mice deficient for Nos3 on a 129/Sv background and in mice deficient for Nos2 on either genetic background. CONCLUSION(S): Our data show that disruption of Nos2 had no effect on ovulation in our mice. The negative effect of Nos3 deficiency on ovulatory capacity and early embryonic development is modulated by genetic background. This suggests a role for strain-specific modifier genes in these processes.

Animals↗
PubMed2006

Genetic background modifies nuclear mutant huntingtin accumulation and HD CAG repeat instability in Huntington's disease knock-in mice.

Genetically precise models of Huntington's disease (HD), Hdh CAG knock-in mice, are powerful systems in which phenotypes associated with expanded HD CAG repeats are studied. To dissect the genetic pathways that underlie such phenotypes, we have generated Hdh(Q111) knock-in mouse lines that are congenic for C57BL/6, FVB/N and 129Sv inbred genetic backgrounds and investigated four Hdh(Q111) phenotypes in these three genetic backgrounds: the intergenerational instability of the HD CAG repeat and the striatal-specific somatic HD CAG repeat expansion, nuclear mutant huntingtin accumulation and intranuclear inclusion formation. Our results reveal increased intergenerational and somatic instability of the HD CAG repeat in C57BL/6 and FVB/N backgrounds compared with the 129Sv background. The accumulation of nuclear mutant huntingtin and the formation of intranuclear inclusions were fastest in the C57BL/6 background, slowest in the 129Sv background and intermediate in the FVB/N background. Inbred strain-specific differences were independent of constitutive HD CAG repeat size and did not correlate with Hdh mRNA levels. These data provide evidence for genetic modifiers of both intergenerational HD CAG repeat instability and striatal-specific phenotypes. Different relative contributions of C57BL/6 and 129Sv genetic backgrounds to the onset of nuclear mutant huntingtin and somatic HD CAG repeat expansion predict that the initiation of each of these two phenotypes is modified by different genes. Our findings set the stage for defining disease-related genetic pathways that will ultimately provide insight into disease mechanism.

Animals↗
PubMed1997

Assessment of learning by the Morris water task and fear conditioning in inbred mouse strains and F1 hybrids: implications of genetic background for single gene mutations and quantitative trait loci analyses.

Genetic methods including the creation of transgenic or null mutant models and mapping studies using quantitative trait loci strategies can be used to identify candidate genes in mice that regulate learning processes. Interpretations as to the impact of single gene mutations for polygenic behaviours like learning will depend in part on the genetic background of the animals used for these manipulations. To address the issue of genetic variability, 12 inbred strains and seven different F1 hybrids were tested on multiple behavioural tasks, including two complex learning paradigms: the Morris water task and fear conditioning. Strain differences were found for all variables measured. In the hidden platform version of the Morris task, the albino animals performed poorly while overall the F1 hybrids showed the best selectivity for the trained quadrant as measured in a probe trial. In contrast, almost all genotypes performed well on the contextual fear conditioning task and learned to associate the test context with the pairing of a foot shock and auditory stimulus as demonstrated 24 h after training by increased freezing in the test environment compared to an altered context. Significant genetic correlations were obtained for behavioural measures suggesting that the same genes regulate various aspects of performance on behavioural tasks. Scores from these multiple inbred strains and F1 hybrids provide a baseline level of learning ability for fear conditioning and the Morris water task. The results of the present study confirm the importance of genetic background in the performance of various learning tasks. This variability should be considered when developing new transgenic or null mutant animal models.

Acoustic Stimulation↗
PubMed2006

Genetic background controls tumor development in PTEN-deficient mice.

PTEN is one of the most frequently mutated tumor suppressor genes in human cancers. Germ line mutations of PTEN have been detected in three rare autosomal-dominant disorders. However, identical mutations in the PTEN gene may lead to different symptoms that have traditionally been described as different disorders, such as Cowden disease, Lhermitte-Duclos disease, and Bannayan-Zonana syndromes. This lack of genotype-phenotype correlation prompted us to directly test the possible effects of genetic background or modifier genes on PTEN-controlled tumorigenesis using genetically engineered mouse models. In this study, we generated two animal models in which either exon 5 (Pten(Delta5)) or promoter to exon 3 (Pten(-)) of the murine Pten gene were deleted and compared phenotypes associated with individual mutations on two genetic backgrounds. We found that the onset and spectrum of tumor formation depend significantly on the genetic background but less on the type of mutation generated. Our results suggest that PTEN plays a critical role in cancer development, and genetic background may influence the onset, the spectrum, and the progression of tumorigenesis caused by Pten mutation.

Alleles↗
PubMed1980

Selective neutrality of 6PGD allozymes in E. coli and the effects of genetic background.

We have used gluconate-limited chemostats to study selective differences between isogenic strains of Escherichia coli K12 into which four naturally occurring alleles coding for allozymes of 6-phosphogluconate dehydrogenase (6PGD) had been transferred. The limit of detectability of selection with our procedures is a selection coefficient of 0.5%. In the normal E. coli K12 genetic background, all alleles are selectively neutral or nearly neutral. The absence of detectable selection does, however, depend on genetic background and on such environmental factors as cell density. In a genetic background containing a mutation that cuts off the alternative metabolic route for 6-phosphogluconate, selection between allozymes can be detected, and the selection is in the direction expected from the measured apparent Km values of the allozymes. Even when the alternative metabolic route is not blocked by mutation, one of the 6PGD allozymes has a detrimental, but density-dependent, interaction with a mutation conferring resistance to bacteriophage T5. In all cases, the observed selection is due to the allozymes themselves (or to associated regulatory elements), as the selection disappears when the chemostats are limited by a different carbon source (ribose plus succinate). Nevertheless, the four alleles do seem to be selectively neutral or nearly neutral in the normal E. coli K12 genetic background. Moreover, the distribution of allele frequencies in natural populations of E. coli is in accord with the expectations of selective neutrality.

Alleles↗
PubMed1986

Lung defenses against Pseudomonas aeruginosa in C5-deficient mice with different genetic backgrounds.

Lung defenses against Pseudomonas aeruginosa were investigated in C5-deficient strains of mice with different genetic backgrounds. We studied pulmonary clearance and cell responses after aerosol exposure to P. aeruginosa in C5-deficient B10.D2/oSnJ and DBA/2J mice and their closest C5-sufficient counterparts, B10.D2/nSnJ and DBA/1J mice. Different patterns of lung clearance and pulmonary cell responses were found for the two C5-deficient strains. C5-deficient B10.D2/oSnJ mice showed defective lung clearance of P. aeruginosa 4 h after challenge compared with C5-sufficient B10.D2/nSnJ animals. This finding was associated with a decreased number of polymorphonuclear leukocytes recruited into the airways during the same time. Interestingly, C5-deficient DBA/2J mice recruited higher numbers of polymorphonuclear leukocytes than did C5-sufficient DBA/1J mice by 4 h after aerosolization. Nevertheless, lung clearance of P. aeruginosa in DBA/2J mice was not as effective as in C5-sufficient DBA/1J mice, suggesting that other functions of C5 besides chemotaxism could be involved. Lung clearance of P. aeruginosa was also investigated in C5-deficient and -sufficient hybrids sharing the same genetic background (DBA/2J X B10.D2). The results suggested that murine lung clearance of P. aeruginosa is markedly affected by lack of C5 in a specific genetic background (B10.D2).

Aerosols↗
PubMed2000

Gender differences in learned helplessness behavior are influenced by genetic background.

Learned helplessness behavior was examined in female and male C57BL/6J (B6), 129/J (129) and (B6 x 129)F1 mice, common genetic backgrounds for the generation of knockout models, as well as in mice of a mixed genetic background (outbred mice). Both genotype and gender differences were observed in learned helplessness. Outbred males showed increased shuttle escape latencies following 60, 120, or 360 inescapable shocks compared to nonshocked controls, but outbred females showed no increase in escape latencies following inescapable shock pretreatment. B6 females showed increased escape latencies following 60, 120, or 360 inescapable shocks, whereas B6 males showed increased latencies only after 360 shocks. Female and male 129 and B6129F1 mice did not show an increase in escape latencies following inescapable shock, but this was most likely due to poor escape performance in nonshocked control mice. Differences in escape performance could not be explained by differences in pain thresholds between genotypes. These results support the idea that genetic background and gender are important to consider when using the learned helplessness model in genetically manipulated mice.

Animals↗
PubMed2002

Complications associated with genetic background effects in models of experimental epilepsy.

To elucidate the genetic influences contributing to susceptibility to seizure disorders, researchers have long used selected lines and inbred strains of rodents. In recent years, the use of genetically altered mice as models of complex human disease has revolutionized biomedical research into the genetics of disease pathogenesis and potential therapeutic interventions. In particular, the study of transgenic and gene-deleted (knockout) mice can provide important insights into the in vivo function and interaction of specific gene products. While a variety of inbred mouse mutations have been used to directly evaluate the genetic basis of seizure disorders, data obtained from such genetically altered mice must be interpreted carefully. An increasing number of scientific articles have reported that the phenotype of a given single gene mutation in mice can be modulated by the genetic background of the inbred strain in which the mutation is maintained. This effect is attributable to so-called modifier genes, which act in combination with the causative gene. In this review, the author points out the importance of considering the genetic background of the strain used to create these animal models, the potential problems with interpretation of phenotype, and solutions to selecting an appropriate mouse model of experimental epilepsy. Despite these potential limitations, knockout mice provide a powerful tool for understanding the genetic and neurobiological mechanisms contributing to experimental epilepsy.

Animals↗
PubMed2003

Allelic diversity in the host genetic background may be an important determinant in tumor metastatic dissemination.

Metastasis, the spread and growth of tumors at secondary sites, is an extremely important clinical event, since the majority of cancer mortality is associated with the metastatic tumors rather than the primary tumor. In spite of the importance of metastasis in the clinical setting, the actual process is extremely inefficient. Millions of tumor cells can be shed into the vasculature daily yet few secondary tumors are formed. To successfully colonize a distant site tumor cells must overcome a series of barriers. Failure to complete any single step in the metastatic cascade abrogates the ability to form a secondary lesion. A variety of theories have been proposed to explain the inefficiency of the metastatic process. The most commonly accepted, the progression theory, posits a series of random mutational occurs within a primary tumor to generate a small subpopulation that acquires full metastatic capability. While significant evidence supports this model, recent discoveries demonstrating the ability to predict metastatic propensity from gene expression profiles in bulk tumor tissue are not consistent with only a small subpopulation of cells in the primary tumor acquiring metastatic ability. A second theory of metastatic inefficiency, the transient compartment theory, is more consistent with the microarray data, but does not completely explain observations like metastasis associated loss-of-heterozygosity events. To reconcile the observed results additional variables need to be added to the model of metastatic inefficiency. One possible variable that might explain the discrepancies is genetic background effects. Studies have demonstrated that the genetic background a tumor arises on can have significant affects on the ability of the tumor to metastasize and on gene expression profiles. Thus the observations could be reconciled by combining the theories, with genetic background influencing both metastatic efficiency and predictive gene expression profiles, upon which subsequently occur metastasis-promoting mutational and epigenetic events. If the genetic background is an important determinant of metastatic efficiency it would have significant implications for the clinical prediction and treatment of metastatic disease, as well as for the design of potential prevention strategies.

Animals↗
PubMed2003

The W303 genetic background affects the isw2 delta mutant phenotype in Saccharomyces cerevisiae.

We performed detailed phenotypic analysis of the isw2 delta strains of the W303 genetic background and compared its results with those obtained previously in BY-derived genetic background. Shmoolike morphology was observed in the isw2 delta strain of alpha-mating type of the BY strains, but not in its W303-derived counterpart. On the other hand, derepression of a-specific genes in the isw2 delta (MAT alpha) strain was observed in both genetic backgrounds, although to a different extent. Unlike in BY-derived strain hyperactivation of the Ras2/cAMP pathway reduced invasiveness of the isw2 delta strain (MAT alpha) of the W303 background. Sensitivity to Calcofluor White indicating a cell wall-integrity defect was significantly increased in the isw2 delta strains of the W303 background in contrast to BY-derived strains. Our data indicate that the effects of the isw2 deletion strongly depend on the background in which the deletion, is made.

Adenosine Triphosphatases↗
PubMed2005

Bayes factor analysis for the genetic background of physiological and vitality variables of F2 Iberian x Meishan newborn piglets.

The Bayes factor (BF) procedure was applied to examine the additive genetic component of several physiological and vitality variables for newborn pigs. Nine variables were studied: heart rate, arterial oxygen saturation, rectal temperature (all at birth and 60 min later), birth weight, interval between birth and first teats contact, and interval between birth and first colostrum intake. The available numbers of data ranged from 288 (heart rate at 60 min) to 839 records (birth weight) from F(2) Iberian x Meishan newborn pigs. We compared a model with zero heritability (nonheritable) with the one where the additive genetic background was included. The BF was used to discriminate between both candidate models. Very strong evidence of genetic background was detected for heart rate 60 min after birth (BF = 48.90), and strong evidence was detected for rectal temperature at birth (BF = 13.82). Posterior modes (means) of heritabilities were 0.29 (0.32) and 0.40 (0.39), respectively. In addition, substantial evidence of absence of genetic background was detected for arterial oxygen saturation at birth.

Animals↗
PubMed1999

[Genetic background in carcinogenesis].

Carcinogenesis comprises both genetic and environmental factors. The genetic factor for cancer is most closely associated with familial cancer. Familial cancer makes up only a few percent of total cancer cases. Recently, various candidate genes for familial cancer have been identified by analyzing patients' family histories and genetically testing them. Most of these cancer susceptibility genes are frequently mutated or deleted on sporadic cancer cells. The study of these genes is very useful for explaining the molecular mechanisms of non-familial cancer. Various polymorphic mutations exist in normal phenotypes in human. Most of them are single nucleotide polymorphisms (SNPs) and intronic variations, but sometimes they are large gene alterations or chromosomal abnormalities. Human genetic polymorphisms can now be more easily analyzed by using computed biotechnology (DNA tips, microarray). Detailed examination of human DNA polymorphisms will advance the study of genetic background in carcinogenesis in the future.

DNA↗
PubMed2004

Modulation of patched-associated susceptibility to radiation induced tumorigenesis by genetic background.

We described previously a basal cell carcinoma (BCC) and medulloblastoma (MB) phenotype for CD1Ptch1(neo67/+) mice exposed to ionizing radiation. Ptch1 heterozygous mice mimic the predisposition to BCC and MB development of patients affected by nevoid BCC syndrome that inherit a mutant Patched (Ptch1) allele. To examine the impact of genetic background on development of BCCs and other tumors we used two outbred mouse lines characterized by extremely high, carcinogenesis-susceptible (Car-S), and low, carcinogenesis-resistant (Car-R), susceptibility to skin carcinogenesis. Crosses between Ptch1(neo67/+) mice and Car-S (F1S) or Car-R mice (F1R) were exposed to ionizing radiation. F1SPtch1(neo67/+) mice were highly susceptible to radiation-induced BCCs, whereas F1RPtch1(neo67/+) mice were completely resistant, indicating that tumor penetrance can be modulated by genetic background. Development of microscopic and macroscopic BCC lesions was influenced by Car-S and Car-R genotypes, suggesting a genetic-background effect on both initiation and progression of BCC. Susceptibility was additionally increased in N2 backcross mice (Car-S x F1SPtch1(neo67/+)), showing a contribution from recessive-acting Car-S modifiers. The modifying effects of Car-S-derived susceptibility alleles were tissue specific. In fact, despite higher susceptibility to BCC induction, Car-S-derived lines had lower MB incidence compared with CD1Ptch1(neo67/+) mice. BCC-associated somatic events were not influenced by genetic background, as shown by similar rate of wild-type Ptch1 loss in BCCs from F1SPtch1(neo67/+) (93%) and CD1Ptch1(neo67/+) mice (100%). Finally, microsatellite analysis of BCCs showed Ptch1 loss through interstitial deletion. These results are relevant to humans, in which BCC is the commonest malignancy, because this model system may be used to study genes modifying BCC development.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2006

Feeling strained? Influence of genetic background on depression-related behavior in mice: a review.

Depression is a growing pandemic in developed societies. The use of inbred mouse strains in pre-clinical psychiatric research has proven to be a valuable resource. Firstly, they provide the background for genetic manipulations that aid in the discovery of molecular pathways that may be involved in major depression. Further, inbred mouse strains are also being used in the determination of genetic and environmental influences that may pre-dispose or trigger depression-related behavior. This review aims to highlight the utility of inbred mouse strains in depression research, while providing an overview of the current state of research into behavioral differences between strains in paradigms commonly used in the field. Neurochemical differences that may underlie strain differences are examined, and some caveats and cautions associated with the use of inbred strains are highlighted.

Animals↗
PubMed2001

Four strains of spontaneously hyperlipidemic (SHL) mice: phenotypic distinctions determined by genetic backgrounds.

Spontaneously hyperlipidemic (SHL) mice are Japanese wild mice (KOR) with disruption of the apolipoprotein E (Apo E) gene. These mice (KOR-Apoe(shl)) are superhypercholesterolemic and develop severe xanthoma, but their atherosclerosis is relatively mild compared with Apo E knockout mice. First, we tested whether this distinction is due to additional mutation of the Apoc1 and/or Apoc2 genes in KOR-Apoe(shl). Southern blot analysis, but found no gross disruption of these genes. Next, we tested whether the phenotypic distinction is due to differences in the genetic background. To this end, we established three lines of congenic SHL mice with a genetic background of C57BL/6, BALB/c or C3H/He, and named them, respectively, C57BL/6.KOR-Apoe(shl) (B6.KOR-Apoe(shl)), BALB/c.KOR-Apoe(shl) (C.KOR-Apoe(shl)) and C3H/He.KOR-Apoe(shl) (C3.KOR-Apoe(shl)). Hypercholesterolemia was most severe in KOR-Apoe(shl) followed the by others as follows; KOR-Apoe(shl)>>C3.KOR-Apoe(shl)>C.KOR-Apoe(shl)>B6.KOR-Apoe(shl). In contrast, atherosclerosis was most severe in B6.KOR Apoe(shl) followed by the others: B6.KOR-Apoe(shl)>C.KOR-Apoe(shl)>>C3.KOR-Apoe(shl)> or =KOR-Apoe(shl). This order, however, did not match that in xanthoma, which was highly prominent in KOR-Apoe(shl) but mild in B6.KOR-Apoe(shl), C.KOR-Apoe(shl) and C3.KORApoe(shl). This order, however, did not match that in xanthoma, which was highly prominant in KOR-Apoe(shl) but mild in B6.KOR-Apoe(shl), C.KOR-Apoe(shl) and C3.KOR-Apoe(shl). These distinctions suggest that the severity of each of the phenotypes is determined by distinct genetic backgrounds which probably are composed of polymorphism of lipid metabolism-related proteins. We found that apolipoprotein A-I is decreased in each SHL strain and polymorphic between B6.KOR-Apoe(shl) and the other strains examined. This polymorphism may be related to the most severe atherosclerosis observed in B6.KOR-Apoe(shl). It is most likely that combination of such polymorphisms is due to the genetic background accountable for phenotype distinctions.

Animals↗
PubMed2003

Phenotype of the zebrafish masterblind (mbl) mutant is dependent on genetic background.

The zebrafish masterblind (mbl) mutant is characterized by the lack of olfactory placodes and optic vesicles, reduced telencephalon, an expanded epiphysis (Heisenberg et al. [1996] Development 123:191-203), and enlarged jaw. To understand the cellular events giving rise to the olfactory placode defect of this mutant, we examined the expression pattern of the distal-less-3 (dlx3) gene in mbl. In the mutant, dlx3, which is normally expressed in the developing nose and ear, showed reduced expression in the olfactory placode field, but normal expression in the developing ear. To determine whether the loss of dlx3 expression was due to cell loss, we assayed cell death by using TUNEL labeling. Although cell death in the mutant was not concentrated in the region of dlx3 expression, there was increased cell death in the forebrain, epiphysis, and jaw region, as compared with that in wild-type controls. This cell death phenotype was cyclical in nature, showing an increase and decrease in cell death on a roughly 24-hr cycle. Further analysis showed that this cyclical phenotype was specific to the genetic background. The severity of the mbl phenotype, including cell death, expanded epiphysis, and enlarged jaw, decreased when the mutation was moved from the original "TL" background to the "AB" background. Thus, the severity of developmental defects in the mbl mutant is strongly dependent on genetic background. We examined the contribution of cell death to the morphologic defects of mbl by blocking cell death by using zVADfmk, a known caspase inhibitor. We found that this treatment partially rescued the expanded jaw defect and that this rescue was dependent on the genetic background. Therefore, the mbl mutant phenotypes result, in part, from genetic background effects that alter the pattern of programmed cell death early in development.

Animals↗
PubMed2000

BRCA2-null embryonic survival is prolonged on the BALB/c genetic background.

Women who inherit mutations in the BRCA2 cancer susceptibility gene have an 85% chance of developing breast cancer. The function of the BRCA2 gene remains elusive, but there is evidence to support its role in transcriptional transactivation, tumor suppression, and the maintenance of genomic integrity. Individuals with identical BRCA2 mutations display a different distribution of cancers, suggesting that there are low-penetrance genes that can modify disease outcome. We hypothesized that genetic background could influence embryonic survival of a Brca2 mutation in mice. Brca2-null embryos with a 129/SvEv genetic background (129(B2-/-)) died before embryonic day 8. 5. Transfer of this Brca2 mutation onto the BALB/cJ genetic background (BALB/c(B2-/-)) extended survival to embryonic day 10.5. These results indicate that the BALB/c background harbors genetic modifiers that can prolong Brca2-null embryonic survival. The extended survival of BALB/c(B2-/-) embryos enabled us to ask whether transcriptional regulation of the Brca1 and Brca2 genes is interdependent. The interdependence of Brca1 and Brca2 was evaluated by studying Brca2 gene expression in BALB/c(B1-/-) embryos and Brca1 gene expression in BALB/c(B2-/-) embryos. Nonisotopic in situ hybridization demonstrated that Brca2 transcript levels were comparable in BALB/c(B1-/-) embryos and wild-type littermates. Likewise, reverse transcriptase-polymerase chain reactions confirmed Brca1 mRNA expression in embryonic day 8.5 BALB/c(B2-/-) embryos that was comparable to Brca2-heterozygous littermates. Thus, the Brca1 and Brca2 transcripts are expressed independently of one another in Brca1- and Brca2-null embryos. Mol. Carcinog. 28:174-183, 2000.

Animals↗
PubMed1996

Expression of Drosophila mushroom body mutations in alternative genetic backgrounds: a case study of the mushroom body miniature gene (mbm).

Mutations in 12 genes regulating Drosophila melanogaster mushroom body (MB) development were each studied in two genetic backgrounds. In all cases, brain structure was qualitatively or quantitatively different after replacement of the "original" genetic background with that of the Canton Special wild-type strain. The mushroom body miniature gene (mbm) was investigated in detail. mbm supports the maintenance of MB Kenyon cell fibers in third instar larvae and their regrowth during metamorphosis. Adult mbm1 mutant females are lacking many or most Kenyon cell fibers and are impaired in MB-mediated associative odor learning. We show here that structural defects in mbm1 are apparent only in combination with an X-linked, dosage-dependent modifier (or modifiers). In the Canton Special genetic background, the mbm1 anatomical phenotype is suppressed, and MBs develop to a normal size. However, the olfactory learning phenotype is not fully restored, suggesting that submicroscopic defects persist in the MBs. Mutant mbm1 flies with full-sized MBs have normal retention but show a specific acquisition deficit that cannot be attributed to reductions in odor avoidance, shock reactivity, or locomotor behavior. We propose that polymorphic gene interactions (in addition to ontogenetic factors) determine MB size and, concomitantly, the ability to recognize and learn odors.

Animals↗