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PubMed2002

Inheritance of resistance to Bt toxin crylac in a field-derived strain of pink bollworm (Lepidoptera: Gelechiidae).

Laboratory selection with Cry1Ac, the Bacillus thuringiensis (Bt) toxin in transgenic cotton, initially produced 300-fold resistance in a field-derived strain of pink bollworm, Pectinophora gossypiella (Saunders), a major cotton pest. After additional selection increased resistance to 3,100-fold, we tested the offspring of various crosses to determine the mode of inheritance of resistance to Cry1Ac. The progeny of reciprocal F1 crosses (resistant male x susceptible female and vice versa) responded alike in bioassays, indicating autosomal inheritance. Consistent with earlier findings, resistance was recessive at a high concentration of Cry1Ac. However, the dominance of resistance increased as the concentration of Cry1Ac decreased. Analysis of survival and growth of progeny from backcrosses (F1 x resistant strain) suggest that resistance was controlled primarily by one or a few major loci. The progression of resistance from 300- to 3,100-fold rules out the simplest model with one locus and two alleles. Overall the patterns observed can be explained by either a single resistance gene with three or more alleles or by more than one resistance gene. The pink bollworm resistance to Cry1Ac described here fits "mode 1" resistance, the most common type of resistance to Cry1A toxins in Lepidoptera.

Animals↗
PubMedDate not supplied

Inherited congenital extrahepatic portosystemic shunts in Cairn terriers.

The pathogenesis of congenital portosystemic shunt (CPSS) in dogs still is incompletely understood. In Irish Wolfhounds and Yorkshire Terriers, CPSS is reported to be hereditary. The aim of this study was to investigate a possible genetic basis and the mode of inheritance of CPSS in Cairn Terriers. Between July 1990 and July 2001, 6-week-old pups of the Dutch Cairn Terrier population were screened by measuring venous ammonia concentrations and in the presence of hyperammonemia by ultrasonography, autopsy, portal vein angiography, or exploratory celiotomy. The same successfully operated female was used 3 times in test matings with an unrelated affected male, her unaffected sire, and an affected offspring. The prevalence of CPSS in the general Cairn Terrier population, the direct progeny of frequently used males, and the offspring of the test matings were tested for significant differences. In total, 6,367 Cairn Terriers were screened; 32 males and 26 females had CPSS. In 3 large family groups, significantly higher prevalences were found compared with the general population (P < .0001, P < .0001, and P < .044). The prevalence of CPSS in the offspring of the test matings was significantly higher (P < .002) than in the general population. No sex predisposition occurred among the affected dogs. The higher prevalence of CPSS in the test matings and the 3 family groups compared with the general population indicates that CPSS in Cairn Terriers is a genetic disease. The inheritance is autosomal and most likely polygenic or monogenic with variable expression.

Animals↗
PubMed2003

Inherited resistance to arsenate toxicity in two populations of Lumbricus rubellus.

No unequivocal evidence exists of genetically inherited resistance to metals/metalloids in field populations of earthworms. We studied cocoon production in adult Lumbricus rubellus Hoffmeister collected from an abandoned arsenic and copper mine (Devon Great Consols, Devon, UK), and abandoned tungsten mine (Carrock Fell, Cumbria, UK) and an uncontaminated cultured population. The earthworms were kept in uncontaminated soil for nine weeks. From a total of 42 L. rubellus from each site, Devon Great Consols adults produced 301 cocoons, of which 42 were viable; Carrock Fell 60 cocoons, of which 11 were viable; and the reference population 101 cocoons, of which 62 were viable. The hatchlings were collected and stored at 4 degrees C at weekly intervals. After 12 weeks, all hatchlings were transferred to clean soil and maintained at 15 degrees C for 20 weeks until they showed evidence of a clitellum. In toxicity trials, F1 generation L. rubellus were exposed to 2,000 mg As/kg as sodium arsenate or 300 mg Cu/kg as copper chloride for 28 d. The F1 generation L. rubellus from Devon Great Consols mine demonstrated resistance to arsenate but not copper. All L. rubellus from Devon Great Consols kept in soil treated with sodium arsenate remained in good condition over the 28-d period but lost condition rapidly and suffered high mortality in soil treated with copper chloride. The control population suffered high mortality in soil treated with sodium arsenate and copper chloride. Previous work has shown that field-collected adults demonstrate resistance to both arsenate and Cu toxicity under these conditions. Thus, while arsenate resistance may be demonstrated in F1 generation L. rubellus from one of the contaminated sites, Cu resistance is not. The F1 adults and F2 cocoons did not have significantly higher levels of As than the control population, with no residual As tissue burden, suggesting that resistance to As in these populations may be inherited.

Adaptation, Physiological↗
PubMed1995

Inheritance of RAPD markers in the guppy fish, Poecilia reticulata.

Random Amplified Polymorphic DNA (RAPD) fingerprinting offers a rapid and efficient method for generating a new series of DNA markers in fishes. Three oligonucleotide primers (two 10-mers and one 9-mer) and their paired combinations were found to generate different but reproducible RAPD fingerprints in the guppy. Of these, a 10-mer primer (designated S3D2) was used to detect DNA polymorphisms in two guppy varieties, Green Snakeskin (GSS) and 3/4Black (3/4B). High Genetic Similarity (SI) was found among individuals of the GSS and 3/4B varieties indicating low intra-variety genetic variability. The average SI values for the Green Snakeskin and 3/4Black varieties were 0.78 +/- 0.104 and 0.81 +/- 0.083, respectively. The average SI value between individuals of the GSS and 3/4B varieties was 0.66 +/- 0.066, indicating higher genetic variability between the two varieties. To study the inheritance of RAPD markers, single-pair crosses were set up between males of the GSS variety and females of the 3/4B variety. The S3D2 primer was used to generate RAPD fingerprints of the parents and their F1 offsprings. A total of 14 RAPD markers were scored from these crosses. Of these markers, eight (60.0%) of them were polymorphic. The RAPD markers were shown by the F1 to exhibit dominant Mendelian inheritance and could thus be used for subsequent genetic linkage mapping of the guppy.

Animals↗
PubMed2002

Inheritance and Interaction of Low Palmitic and Low Linolenic Soybean.

Decreasing the palmitic and linolenic acid content of soybean [Glycine max (L.) Merrill] oil would help improve its nutritional quality and oxidative stability. The altered fatty acid profile in soybean germplasm lines with decreased levels of palmitic and linolenic acid have been developed at the University of Guelph, Canada, by combining different mutant alleles through hybridization. The objectives of this study were to determine the inheritance and interaction of palmitic and linolenic acid levels in RG3 and RG1, and the effects of these altered fatty acid levels on other fatty acids. RG3 and RG1 (low palmitic approximately 45 g kg(-1) and linolenic approximately 40 g kg(-1)) were crossed reciprocally to several soybean lines with altered or normal fatty acid profiles. Analysis of the reciprocal F(2) generations indicated no maternal or cytoplasmic effects for palmitic or linolenic acid content. Chi-square analyses of the F(2) generation demonstrated that RG3 and RG1 contained two alleles, fap1 and fapx, that controlled palmitic acid content. In addition, RG1 had a third allele, fan, which reduced its linolenic acid content. Calculation of gene substitution values indicated additive gene action at the fap1 and fan loci, whereas the fapx locus involved partial dominance. Correlation coefficients indicated no association between palmitic and linolenic acid. Decreases in palmitic and linolenic acid content were associated primarily with increases in linoleic acid content. Since fap1, fapx, and fan were inherited independently of each other and appeared to behave in an additive manner, RG3 and RG1 can be used in breeding programs as additional valuable sources of germplasm with altered fatty acid profiles.

Journal Article↗
PubMed2006

RNA based gene therapy for dominantly inherited diseases.

There are numerous examples in the literature of gene therapy applications for recessive disorders. There are precious few instances, however, of studies conducted to treat dominantly inherited pathologies. The reasons are simple: there are fewer cases of dominantly inherited diseases on one hand, but mostly it is far easier to correct recessive mutations than dominant ones. Typically recessive mutations cause a loss of (or reduced) gene function which can be compensated for by introduction of a replacement allele into the cell. In contrast, dominant negative mutations not only display impaired function, but also exhibit a novel one that is pathologic to the cell. Treating these conditions by gene therapy implies silencing the dominant allele without altering the expression of the wild-type gene. We describe here different strategies aimed at silencing dominant mutations through mRNA destruction and provide examples of their application to known autosomal dominant diseases. An overview of the most common molecular tools (antisense DNA and RNA, ribozymes and RNA interference) suitable to utilize these strategies is also presented and we discuss the relevant aspects involved in the choice of a particular approach in a gene therapy experiment.

Animals↗
PubMedDate not supplied

[Gene transfer as treatment for metabolic inherited liver diseases]

OBJECTIVE: To study gene transfer looking for its future clinical application in the treatment of metabolic inherited liver diseases. METHODS: Bibliographic review about the subject. RESULTS AND CONCLUSIONS: Gene transfer into the liver would be an alternative to liver transplantation to treat some inherited metabolic diseases. Various vectors have been employed for gene transfer, including retrovirus vectors, whose integration into the chromosomal DNA would allow stable long term expression of the transgene. The integration of retrovirus vectors into the genoma of the target cell is only possible during mitosis. Therefore, these vectors must be delivered during hepatic regeneration induced by partial hepatectomy, for example. Another obstacle to be overcome is the extra hepatic dissemination of retrovirus, in particular to the germinals cells, due to the risk of changing the genetical heritage of the progeniture.

Journal Article↗
PubMed1980

Racial differences in juvenile-type diabetes are consistent with more than one mode of inheritance.

The ratio of the prevalences of insulin-dependent type (juvenile) diabetes (IDDM) in blacks and Caucasians is examined. It has been argued that this ratio is of the same order as the estimated proportion of Caucasian genes in the American black population. It has been further argued that this observation, together with an assumption of equal penetrances in the two races, is consistent with autosomal dominant inheritance for IDDM. The present paper shows that the ratio is equally compatible with a three-allele model which, moreover, incorporates observed immunogenetic heterogeneity within IDDM. This three-allele heterogeneity model exhibits some features of both dominant and recessive inheritance. The model predicts that, compared with Caucasians, there will be less pancreatic autoimmunity in the black IDDM population and lower recurrence risks to relatives of black diabetics. These predictions can be tested in future studies.

Alleles↗
PubMed1994

Maternally inherited diabetes and deafness is a distinct subtype of diabetes and associates with a single point mutation in the mitochondrial tRNA(Leu(UUR)) gene.

We have recently reported an A to G transition at nucleotide position 3243 in the mitochondrial DNA (mtDNA) tRNA(Leu(UUR)) gene in a large family with non-insulin-dependent diabetes mellitus (NIDDM). Characteristic was its maternal transmission and an associated sensorineural hearing loss. In a screening of a Dutch and French NIDDM population for the presence of the tRNA(Leu(UUR)) mutation we identified two new pedigrees in which NIDDM is present in combination with deafness. The mode of inheritance agrees with a maternal one. This result shows that patients with a phenotype of NIDDM and deafness can be identified within groups of NIDDM patients based on the tRNA(Leu(UUR)) mutation. The same mutation has also been linked to the syndrome of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). How the same mutation can give rise to different clinical phenotypes is not clear. We obtained the complete mtDNA sequence from our initial pedigree and identified a number of additional mutations that could confer the phenotype of the tRNA(Leu(UUR)) mutation to diabetes. We examined the presence of these additional, potentially pathogenic mutations in the mtDNA from the two new pedigrees and from a previously described British pedigree. The absence of these mutations in all three pedigrees shows that the tRNA(Leu(UUR)) mutation alone associates with the phenotype of NIDDM and deafness. We conclude that maternally inherited diabetes and deafness is a distinct subtype of diabetes that is associated with a single mitochondrial tRNA(Leu(UUR)) mutation. We propose the abbreviation MIDD for this particular subtype.

Base Sequence↗
PubMed1999

Hyperinsulinism caused by paternal-specific inheritance of a recessive mutation in the sulfonylurea-receptor gene.

Neonatal hyperinsulinism (HI) is a genetic disorder of pancreatic beta-cells characterized by failure to suppress insulin secretion in the presence of hypoglycemia, resulting in brain damage or death if not adequately treated. Germline mutations in four genes have been associated with HI. Some patients have focal regions of beta-cell proliferation (focal HI). Seventy HI probands in whom at least one SUR-1 mutation was identified were studied. Clinical data from patients with two SUR-1 mutant alleles were compared with those from patients with single paternally inherited mutations. Thirty-seven probands were homozygous or compound heterozygous for SUR-1 mutations. In 33 probands, only a single mutation was identified, and in 31, the parental origin of the proband could be determined; in 29, the mutation was on the paternal allele (P < 0.0002). For three of these, pancreatic tissue was available and showed focal beta-cell hyperplasia. DNA extracted from the focal lesion and adjacent normal pancreas revealed loss of the maternal chromosome 11p15, resulting in reduction to homozygosity for the SUR-1 mutation within the focal lesion only. Using the Tdt-mediated dUTP nick end labeling (TUNEL) reaction, apoptotic beta-cells were identified exclusively within the focal region. At diagnosis, disease severity was similar in patients with paternally inherited mutations and those with two mutations. For patients who did not undergo surgery, those with only paternal mutations entered clinical remission within 16 +/- 6.2 months, compared with 48 +/- 23 months for those with two SUR-1 mutations (P = 0.001). In conclusion, we identified a novel mechanism to explain the pathophysiology of focal HI and provide evidence to suggest that this entity may be self-limiting, since affected beta-cells undergo apoptosis.

ATP-Binding Cassette Transporters↗
PubMed2000

Inheritance of von Willebrand's disease in a colony of Doberman Pinschers.

OBJECTIVE: To determine the mode of inheritance of von Willebrand's disease (vWD) and perform linkage analysis between vWD and coat color or narcolepsy in a colony of Doberman Pinschers. ANIMALS: 159 Doberman Pinschers. PROCEDURE: von Willebrand factor antigen (vWF:Ag) concentration was measured by use of ELISA, and results were used to classify dogs as having low (< 20%), intermediate (20 to 65%), or high (> 65%) vWF:Ag concentration, compared with results of analysis of standard pooled plasma. Buccal bleeding time was measured, and mode of inheritance of vWD was assessed by pedigree analysis. RESULTS: von Willebrand's disease was transmitted as a single autosomal gene defect. Results suggested that 27.04% of dogs were homozygous for vWD, 62.26% were heterozygous, and 10.69% did not have the defect. Most homozygous and some heterozygous dogs had prolonged bleeding times. Dogs with diluted coat colors (blue and fawn) were significantly overrepresented in the homozygous group, compared with black and red dogs, but a significant link between vWD and coat color was not detected. CONCLUSIONS AND CLINICAL RELEVANCE: von Willebrand's disease is transmitted as an autosomal dominant trait with variable penetrance; most dogs in this colony (89.3%) were carriers of vWD. Homozygosity for vWD is not likely to be lethal. Some heterozygous dogs have prolonged bleeding times. An association between diluted coat colors and vWD may exist.

Animals↗
PubMed2000

Inheritance of gluten-sensitive enteropathy in Irish Setters.

OBJECTIVE: To establish a model for inheritance of gluten-sensitive enteropathy (GSE) in Irish Setters. ANIMALS: 44 dogs of a 6-generation family of Irish Setters with GSE and 7 healthy Irish Setters. PROCEDURE: Phenotype of each dog was determined after oral administration of gluten in the weaning diet, using morphometric evaluation of jejunal biopsies (all generations) and measurement of small intestinal permeability by use of a lactulose-rhamnose permeation test (generations 1, 2, and 3). Overall probability for each of 4 genetic models of inheritance (autosomal recessive, autosomal dominant, sex-linked recessive, and sex-linked dominant) accounting for segregation of partial villus atrophy within the entire family was calculated. RESULTS: The autosomal recessive model was most tenable and was 56,250 times more likely to account for segregation of partial villus atrophy than the autosomal dominant model, assuming disease prevalence of 0.8%. Both sex-linked models were untenable. These conclusions were robust to the error attached to estimation of disease prevalence. High intestinal permeability without morphometric jejunal abnormalities in 4 of 20 dogs in the 3 youngest generations suggested heterogeneity of lesions associated with GSE. CONCLUSIONS: Genetic transmission of GSE is under the control of a single major autosomal recessive locus.

Animals↗
PubMed1997

Phenotypic characterization of rambouillet sheep expressing the callipyge gene: I. Inheritance of the condition and production characteristics.

The objectives of this study were to determine the model of inheritance of the callipyge gene and to evaluate the growth, ADFI, feed efficiency, reproductive performance, and wool growth of sheep that are heterozygous for the callipyge gene. Ewes (n = 236) with a normal muscle phenotype and genotype were mated to three heterozygous rams that expressed the callipyge gene. Lambs (n = 311) were subjectively classified at weaning (90 to 120d) according to muscle phenotype by a panel of three evaluators working independently. The callipyge muscle phenotype was expressed in 150 lambs, whereas 161 lambs expressed a normal muscle phenotype. The percentage of lambs expressing the callipyge muscle phenotype (48.2%) did not differ (P > .1) from the expected 50%. Growth rate was similar for lambs of both phenotypes regardless of sex. Feed efficiency was superior (P < .05) for both male and female lambs with the callipyge muscle phenotype. Average daily feed intake was lower for male (P < .02) and female (P < .004) lambs with the callipyge muscle phenotype. Grease fleece weight and staple length at 12 mo were superior (P < .03) for ewes with a normal muscle phenotype. These results indicate that the callipyge gene in sheep is dominant when inherited from the paternal parent and lambs expressing the callipyge gene have increased feed efficiency and reduced ADFL.

Animals↗
PubMed1999

The callipyge phenomenon: evidence for unusual genetic inheritance.

In 1983, a male lamb exhibiting a pronounced muscular hypertrophy, particularly noticeable in the hind quarters, was born into a commercial Dorset flock in Oklahoma. The ram was premonitorily called Solid Gold. He subsequently produced offspring expressing the unusual phenotype, which is referred to as callipyge (Greek: calli- beautiful + -pyge buttocks). Animals demonstrating the callipyge phenotype are all descendants of this founder ram. These animals produce leaner, higher yielding carcasses, but there is some concern with decreased tenderness of the loin. Genetic characterization of the locus has demonstrated a unique mode of inheritance termed polar overdominance, in which only heterozygous offspring inheriting the mutation from their sire express the phenotype. The three other genotypes are normal in appearance. Progeny data indicate that reactivation of the maternal callipyge allele occurs after passage through the male germ line, although this reactivation is not absolute. The callipyge gene has been mapped to the distal end of ovine chromosome 18.

Animals↗
PubMed2001

The effects of Piedmontese inheritance and myostatin genotype on the palatability of longissimus thoracis, gluteus medius, semimembranosus, and biceps femoris.

The objective of this study was to determine the relative contributions of Piedmontese inheritance (0, 25, 50, or 75%) and myostatin genotype (+/+, mh/+, and mh/mh) to tenderness of four major muscles. Matings were made to produce animals with 0 (+/+), 1 (mh/+), or 2 (mh/mh) inactive myostatin alleles that were known to result in normal muscling, heavy muscling, and extremely heavy muscling, respectively. Over a 4-yr period, 395 steers and heifers (14 to 17 mo of age) were humanely slaughtered and the carcasses were chilled 48 h at 0 degrees C. An eight-member trained descriptive attribute panel evaluated tenderness, ease of fragmentation, connective tissue amount, juiciness, and beef flavor intensity of longissimus thoracis (LD), gluteus medius (GM), semimembranosus (SM), and biceps femoris (BF) steaks at 14 d postmortem. Data were analyzed for the main effects of group (eight combinations of myostatin genotype and percentage Piedmontese; [+/+]/0%, [+/+]/25%, [+/+]/50%, [mh/+]/25%, [mh/+]/50%, [mh/+]/75%, [mh/mh]/50%, [mh/mh]/75%) and muscle. Muscle x group interactions were not significant (P > 0.05). Within myostatin genotypes, contrasts to test the effect of percentage Piedmontese were not significant (P > 0.05). Data were reanalyzed for the main effects of myostatin genotype and muscle. Tenderness, ease of fragmentation, and amount of connective tissue ratings were higher (P < 0.05) for the mh/+ and mh/mh genotypes relative to +/+ in all muscles. In biceps femoris, mh/mh had higher (P < 0.05) tenderness, ease of fragmentation, and amount of connective tissue ratings than the mh/+ genotype. Juiciness ratings were lower (P < 0.05) for mh/mh than for mh/+ in all muscles and were lower for mh/mh than for +/+ in all muscles except gluteus medius. Beef flavor intensity ratings were lower (P < 0.05) for mh/mh than for +/+ in all muscles. Muscle ranks for tenderness within myostatin genotype were LD > GM > SM > BF, LD > GM > SM > BF, LD > GM > BF > SM, for +/+, mh/+, and mh/mh genotypes, respectively. The effects of Piedmontese inheritance on meat tenderness were all due to myostatin genotype. Piedmontese mh/mh bulls could be used as terminal sires to produce mh/+ progeny with improved carcass value due to improved tenderness in the four muscles studied.

Animals↗
PubMed1996

A preliminary study on inherited tooth morphology characters of Japanese and Chinese young adults--with special reference to the Carabelli tubercle.

A comparative study on inherited tooth morphology characters, in particular the incidence of Carabelli tubercles in the maxillary dentition, was conducted on standardized stone casts obtained from 240 Japanese (124 males (male) and 116 females (females)) and 160 Chinese (74 male, 86 female) young adults. The following results were obtained: 1) No significant differences in the incidence of Carabelli tubercles according to sex or body height were found between the two groups. 2) However, significant differences in the incidence of Carabelli tubercles according to sex were found in both groups. The tubercles occurred more frequently in males. 3) Significant differences between the bilateral and unilateral occurrence of Carabelli tubercles were observed in both the Japanese (p < 0.05) and Chinese (p < 0.01) groups; Carabelli tubercles on upper first molars were always bilateral. 4) The highest incidence of Carabelli tubercles was found in individuals with a body height of 166 approximately 175 cm in both groups, and a significant difference (p < 0.05) between the 156 approximately 165 cm and 166 approximately 175 cm groups was particularly evident in the Japanese adults. The authors postulate that bilateral occurrence of Carabelli tubercles was originally an inherited character in the molar region, but that the character was inhibited during the process of evolution of the masticatory system and regression of the molar dentition.

Adult↗
PubMedDate not supplied

inheritance of sperm centrioles and centrosomes in bovine embryos.

Immature cumulus oocyte complexes (COCs) were aspirated from ovarian follicles of slaughtered cow and matured for 24 h in TCM 199 medium with hormones. Eighty-five percent of oocytes matured with subsequent abstriction of the polar body. Matured COCs were then inseminated with frozen-thawed semen (2 x 10(6)/mL final concentration). Eighteen hours after insemination, fertilized COCs were vortexed, washed, and cultured to the pronuclear stage and syngamy (24-36 h postinsemination) and fixed for TEM. Unfixed embryos achieved a cleavage rate of 54%, with 29% developing to blastocysts. Fertilization was confirmed by TEM. Examination of fertilized bipronuclear ova revealed the presence of a sperm aster associated with sperm midpieces, tails, and male pronuclei in several embryos. Further examination of embryos at syngamy showed centrioles at one pole of the first mitotic bipolar spindle in two embryos. Since the mature oocyte at metaphase II has no centrioles at spindly poles, this centriole was most likely derived from the sperm, which has a single proximal centriole associated with pericentriolar material in its neck region, like most mammalian sperm. Tripronuclear ova produced disorganized bipolar spindles or, rarely, tripolar spindles. Bovine embryos, too, follow Boveri's rule of paternal inheritance as in man and most animals. It is possible that both paternal centrosomes (centrioles) and maternal centrosomes are involved in the organization of bipolar spindles in these embryos, quite unlike the mouse embryo where maternal centrosomes seem to organize the first mitotic spindle. The bovine embryo appears to be an appropriate model to study centriolar inheritance.

Animals↗
PubMed1984

The mode of inheritance of a defect in lamination in the hippocampus of BALB/c mice.

In BALB/c mice the lamination of the pyramidal cell layer of area CA3c of the hippocampus is abnormal in that early-generated neurons are superficial and late-generated neurons are deep. To determine the mode of inheritance of this strain difference, the laminar distribution of mossy fibers and hippocampal pyramidal cells was examined using the Timm's sulfide silver method in BALB/c x C57BL/6 F1 and F2 hybrids, in BALB/cByJ and C57BL/6J mice which were fostered to females of the other strain before receiving their first meal, and in the CXB series of recombinant inbred strains (originally derived using BALB/c and C57BL/6 as progenitor strains). The pattern of hippocampal lamination was classified as "BALB/c-like" if pyramidal cells were present below an intrapyramidal mossy fiber layer or as "B6-like" if only an infrapyramidal mossy fiber layer was present. In both male and female CB6F1 and B6CF1 hybrids the distribution of mossy fibers is BALB/c-like. In 7 of 9 F2 hybrids the distribution was BALB/c-like and in the remaining 2 B6-like. In the cross-fostered mice the pattern was always the same as normally raised mice of the same genotype. Of the recombinant inbred strains, 5 (CXBD, CXBG, CXBH, CXBI, and CXBK) had BALB/c-like hippocampal lamination and 2 (CXBE and CXBJ) had B6-like lamination. These results are consistent with inheritance by means of a single autosomal dominant (or semi-dominant) gene. The provisional name "Hippocampal lamination defect" and gene symbol Hld are suggested. The Hld mutation is only the third known neurological mutation in mice which apparently affects neuronal migration, and the fact that it affects only a single subdivision of the hippocampus indicates that Hld may be a useful tool for future studies of the development of the central nervous system and particularly of the cell biology of neuronal migration and neuronal specificity.

Animals↗