Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Genetic background”

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 883 records · Page 49Linked to original sources
PubMed2006

Mutation accumulation in the intestine and colon of mice deficient in two intracellular glutathione peroxidases.

Mice deficient in two glutathione peroxidases (GPX), Gpx1 and Gpx2, [Gpx1/2-double knockout (DKO) mice] are prone to ileocolitis on a mixed C57BL/6 and 129S1/SvJ (B6.129) genetic background. We reported previously that approximately 25% of B6.129 Gpx1/2-DKO mice develop ileocolonic tumors by 6 to 9 months of age, when their non-DKO littermates [having at least one wild-type (WT) Gpx1 or Gpx2 allele] rarely have inflammation and none have tumors. Because genetic background affects tumor susceptibility, we have generated a B6 Gpx1/2-DKO colony and discovered that these mice have fewer inflammatory cells, milder ileocolitis, and low mortality, and only 2.5% of B6 mice developed tumors. The mutant frequency of a cII reporter gene was about 2- to 3-fold higher in 28-day-old Gpx1/2-DKO and 4-fold higher in 8-month-old Gpx1/2-DKO ileal mucosa than in controls in both genetic backgrounds. In contrast, mutant frequencies in the unaffected B6 liver were not significantly different between WT and Gpx1/2-DKO mice. The mutant frequency of 8-month-old B6.129 Gpx1/2-DKO ileum was 38.94 +/- 15.5(-5), which was not significantly higher than the age-matched B6 ileum, 25.54 +/- 10.33(-5). The mutation spectra analysis has shown that B6 Gpx1/2-DKO ileum had a 3-fold increase in small nucleotide deletions at mononucleotide repeats over control B6, which are a signature mutation associated with oxidative stress. Unexpectedly, B6 Gpx1/2-DKO mice had fewer C to T transitions at CpG dinucleotides than the WT B6 (18.0% versus 40.1%; P < 0.001). Our results suggest that inflammation drives gene mutations, which leads to neoplastic transformation of intestinal epithelium in the B6.129 Gpx1/2-DKO mice but rarely in the B6 Gpx1/2-DKO mice.

Animals↗
PubMed2006

HIV-1 genes vpr and nef synergistically damage podocytes, leading to glomerulosclerosis.

This study aimed to identify the causative gene for HIV-1 associated nephropathy, a paradigmatic podocytopathy. A previous study demonstrated that transgenic expression of nonstructural HIV-1 genes selectively in podocytes in mice with FVB/N genetic background resulted in podocyte injury and glomerulosclerosis. In this study, transgenic mice that expressed individual HIV-1 genes in podocytes were generated. Five of six transgenic mice that expressed vpr developed podocyte damage and glomerulosclerosis. Analysis of an established vpr transgenic line revealed that transgenic mice on FVB/N but not on C57BL/6 genetic background developed podocyte injury by 8 wk of age, with later glomerulosclerosis. Four of 11 transgenic mice that expressed nef also developed podocyte injury. One transgenic line was established from the nef founder mouse with the mildest phenotype. Transgenic mice in this line developed mesangial expansion at 3 wk of age and mild focal podocyte damage at 10 wk of age. Mating with FVB/N mice did not augment nephropathy. None of the transgenic mice that expressed vif, tat, rev, or vpu in podocytes, even with the FVB/N genetic background, developed podocyte injury. For testing effects of simultaneous expression of vpr and nef, these two lines were mated. All nef:vpr double-transgenic mice showed severe podocyte injury and glomerulosclerosis by 4 wk of age. In contrast, all vpr or nef single-transgenic mice in the same litter uniformly showed no or much milder podocyte injury. These findings indicate that vpr and nef each can induce podocyte injury with a prominent synergistic interaction.

AIDS-Associated Nephropathy↗
PubMed2004

The use of animal models in the study of complex disease: all else is never equal or why do so many human studies fail to replicate animal findings?

The study of the genetics of complex human disease has met with limited success. Many findings with candidate genes fail to replicate despite seemingly overwhelming physiological data implicating the genes. In contrast, animal model studies of the same genes and disease models usually have more consistent results. We propose that one important reason for this is the ability to control genetic background in animal studies. The fact that controlling genetic background can produce more consistent results suggests that the failure to replicate human findings in the same diseases is due to variation in interacting genes. Hence, the contrasting nature of the findings from the different study designs indicates the importance of non-additive genetic effects on human disease. We discuss these issues and some methodological approaches that can detect multilocus effects, using hypertension as a model disease. This article contains supplementary material, which may be viewed at the BioEssays website at http://www.interscience.wiley.com/jpages/0265-9247/suppmat/index.html.

Animals↗
PubMedDate not supplied

Preferential selection of specific rotavirus gene segments in coinfection and multiple passages with reassortant viruses and their parental strain.

We previously reported non-random selections of human rotavirus (HRV) Wa genes 2 and 5 in reassortant formation between HRV strains Wa and HN126 under selection pressure with neutralizing monoclonal antibodies. In order to study whether or not these genes are preferentially selected in the genetic background of a parental strain HN126 in vitro without selection pressures, coinfection and multiple passage experiments were performed between HN126 and one of three reassortants, C1, C1T and C1F; C1 possessed genes 2 and 5 derived from Wa and the other genes derived from HN126, while C1T and C1F were single gene reassortants having Wa gene 2 or Wa gene 5 in the genetic background of HN126, respectively. When MA-104 cells were coinfected with the same infectious units of HN126 and C1, Wa genes 2 and 5 of reassortant C1 became predominant within 10 repeated passages, although Wa gene 5 was selected more preferably than Wa gene 2. Similar results were obtained under different experimental conditions in which different doses of parental strains or different type of cells were used. Also, in coinfections of MA-104 cells with HN126 and C1T, or HN126 and C1F, Wa gene 2 or Wa gene 5 became predominant at the sixth passage. Analysis of viral growth curves indicated that two reassortants, C1 and C1F, replicated to a titre higher than HN126, while no difference in viral growth was observed between C1T and HN126. These results indicated that in the genetic background of HN126, Wa gene 5 might provide viruses with a growth advantage compared with its HN126 counterpart, while Wa gene 2 might be preferentially selected into reassortant clones through its greater functional capacity for assortment during viral replication.

Animals↗
PubMed1998

Relative paucity of genes causing inviability in hybrids between Drosophila melanogaster and D. simulans.

Using deficiencies from Drosophila melanogaster, we looked for genomic regions in the sister species D. simulans that could cause lethality when hemizygous on a hybrid genetic background. Such genotypes allow hemizygous genes from one species to interact with heterozygous genes from other species and may correspond to the kinds of genotypes causing Haldane's rule, the observation that if only one gender is sterile or inviable in species hybrids, it is nearly always the heterogametic sex. A survey of roughly 50% of the D. simulans genome (114 chromosome regions) revealed only four regions causing hybrid lethality and five causing severe reductions in hybrid viability. However, the viability of all of these genotypes was at least partially restored by rearing hybrids at lower temperature or using different genetic backgrounds from D. simulans. We therefore detected no D. simulans chromosome regions causing unconditional hybrid lethality, although several regions were shown to be deleterious under most tested temperatures and genetic backgrounds. The relative paucity of "inviability genes" supports the idea, suggested by work on other species, that hybrid inviability between closely related species might be caused by interactions among relatively few genes, while hybrid sterility may involve many more loci.

Animals↗
PubMed1999

The yeast ras/cyclic AMP pathway induces invasive growth by suppressing the cellular stress response.

Haploid yeast cells are capable of invading agar when grown on rich media. Cells of the Sigma1278b genetic background manifest this property, whereas other laboratory strains are incapable of invasive growth. We show that disruption of the RAS2 gene in the Sigma1278b background significantly reduces invasive growth but that expression of a constitutively active Ras2p (Ras2(Val19)p) in this strain has a minimal effect on its invasiveness. On the other hand, expression of Ras2(Val19)p in another laboratory strain, SP1, rendered it invasive. These results suggest that a hyperactive Ras2 pathway induces invasive growth and that this pathway might be overactive in the Sigma1278b genetic background. Indeed, cells of the Sigma1278b are defective in the induction of stress-responsive genes, while their Gcn4 target genes are constitutively transcribed. This pattern of gene expression was previously shown to be associated with an active Ras/cyclic AMP (cAMP) pathway. We show that suppression of stress-related genes in Sigma1278b cells is a result of their inability to activate transcription through the stress response element (STRE). Disruption of RAS2, which abolished invasiveness, induced an increase in STRE activity. Further, in the SP1 genetic background, disruption of either the MSN2/4 genes (encoding activators of STRE) or the yAP-1 gene was sufficient to restore invasive growth in ras2Delta cells. We conclude that Ras2-mediated suppression of the stress response is sufficient to induce invasiveness. Accordingly, the fact that the stress response is suppressed in Sigma1278b background explains its invasiveness. It seems that invasiveness is a phenotype related to unregulated growth and is therefore manifested by cells harboring an overactive Ras/cAMP cascade. In this respect, invasiveness in yeast is reminiscent of the property of ras-transformed fibroblasts to invade soft agar.

Cell Differentiation↗
PubMed2003

Use of a novel outbred by inbred F1 cross to detect genetic markers for growth.

A unique outbred by inbred F1 resource population was established. The population structure facilitated the unique opportunity of examining gene by genetic background interaction through crossing two modern broiler sires with dams from two unrelated inbred lines, with no selection for growth rate, to produce about 600 F1 chicks. Pools of DNA were generated from the phenotypic extremes (20% high and low) for 8-week body weight for each of the four combinations of sire and dam line. For one sire family, pools were also separately generated for each sex. The pools were genoyped with 25 informative (segregating) microsatellites. This unique F1 cross between outbred and inbred populations allowed use of the inbred alleles as an 'internal control' for polymerase chain reaction amplification quality in DNA pools. Ten microsatellites showed marked differences (P < 0.05) in allele frequencies between high and low pools, suggesting an association between marker and quantitative trait loci (QTL). These differences were verified using selective genotyping. For many markers, differences in allele frequencies between the high and the low pools, or marker effect, varied between the two dam lines and the two sexes, suggesting an interaction between some genes and the genetic background as represented by different dam lines or sexes. The suggestive marker-QTL associations identified in this F1 population demonstrate the efficiency of this population design while different QTL effects in different genetic line crosses and sexes highlight the importance of gene by genetic background interaction in QTL detection.

Animals↗
PubMed2003

Analysis of the embryonic phenotype of Bent tail, a mouse model for X-linked neural tube defects.

Neural tube defects, mostly believed to result from closure defects of the neural tube during embryonic development, are frequently observed congenital malformations in humans. Since the etiology of these defects is not well understood yet, many animal models for neural tube defects, either arising from spontaneous mutations or generated by gene targeting, are being studied. The Bent tail mouse is a model for X-linked neural tube defects. This mutant has a characteristic short and kinked tail. Exencephaly occurs in Bent tail embryos with a frequency of 11-16%. Laterality defects also belong to the phenotypic spectrum. In this study, we analyzed the embryonic phenotype in further detail using scanning electron microscopy during the stages of neurulation. We observed a number of defects in both wild type and Bent tail embryos, including a kinked neural tube, tight amnion, delay in axial rotation and even malrotation. The severity or frequency of most defects, the delay in axial rotation excluded, was significantly higher in Bent tail embryos compared to wild type embryos. Other abnormalities were seen in Bent tail embryos only. These defects were related to anterior and posterior neural tube closure and resulted in exencephaly and a closure delay of the posterior neuropore, respectively. The exencephalic phenotype was further analyzed by light microscopy in ED14 embryos, showing disorganization and overgrowth in the mesencephalon and rhombencephalon. In conclusion, the anterior and posterior neural tube closure defects in the Bent tail are strictly linked to the genetic defect in this mouse. Other phenotypic features described in this study also occur in the wild type genetic background of the Bent tail strain. Apparently, the genetic background contains elements conducive to these developmental abnormalities.

Animals↗
PubMed2004

Analysis of T-DNA- Xa21 loci and bacterial blight resistance effects of the transgene Xa21 in transgenic rice.

The genetic loci and phenotypic effects of the transgene Xa21, a bacterial blight (BB) resistance gene cloned from rice, were investigated in transgenic rice produced through an Agrobacterium-mediated transformation system. The flanking sequences of integrated T-DNAs were isolated from Xa21 transgenic rice lines using thermal asymmetric interlaced PCR. Based on the analysis of 24 T-DNA- Xa21 flanking sequences, T-DNA loci in rice could be classified into three types: the typical T-DNA integration with the definite left and right borders, the T-DNA integration linked with the adjacent vector backbone sequences and the T-DNA integration involved in a complicated recombination in the flanking sequences. The T-DNA integration in rice was similar to that in dicotyledonous genomes but was significantly different from the integration produced through direct DNA transformation approaches. All three types of integrated transgene Xa21 could be stably inherited and expressed the BB resistance through derived generations in their respective transgenic lines. The flanking sequences of the typical T-DNA integration consisted of actual rice genomic DNA and could be used as probes to locate the transgene on the rice genetic map. A total of 15 different rice T-DNA flanking sequences were identified. They displayed restriction fragment length polymorphisms (RFLPs) between two rice varieties, ZYQ8 and JX17, and were mapped on rice chromosomes 1, 3, 4, 5, 7, 9, 10, 11 and 12, respectively, by using a double haploid population derived from a cross between ZYQ8 and JX17. The blast search and homology comparison of the rice T-DNA flanking sequences with the rice chromosome-anchored sequence database confirmed the RFLP mapping results. On the basis of genetic mapping of the T-DNA- Xa21 loci, the BB resistance effects of the transgene Xa21 at different chromosome locations were investigated using homozygous transgenic lines with only one copy of the transgene. Among the transgenic lines, no obvious position effects of the transgene Xa21 were observed. In addition, the BB resistance levels of the Xa21 transgenic plants with different transgene copy numbers and on different genetic backgrounds were also investigated. It was observed that genetic background (or genome) effects were more obvious than dosage effects and position effects on the BB resistance level of the transgenic plants.

Base Sequence↗
PubMed2003

Genome-wide patterns of expression in Drosophila pure species and hybrid males.

One of the most fundamental questions for understanding the origin of species is why genes that function to cause fertility in a pure-species genetic background fail to produce fertility in a hybrid genetic background. A related question is why the sex that is most often sterile or inviable in hybrids is the heterogametic (usually male) sex. In this survey, we have examined the extent and nature of differences in gene expression between fertile adult males of two Drosophila species and sterile hybrid males produced from crosses between these species. Using oligonucleotide microarrays and real-time quantitative polymerase chain reaction, we have identified and confirmed that differences in gene expression exist between pure species and hybrid males, and many of these differences are quantitative rather than qualitative. Furthermore, genes that are expressed primarily or exclusively in males, including several involved in spermatogenesis, are disproportionately misexpressed in hybrids, suggesting a possible genetic cause for their sterility.

Animals↗
PubMed2005

Expression of HIV-1 genes in podocytes alone can lead to the full spectrum of HIV-1-associated nephropathy.

BACKGROUND: Human immunodeficiency virus (HIV)-1-associated nephropathy (HIVAN) is characterized by collapsing focal and segmental glomerulosclerosis (FSGS) and microcystic tubular dilatation. HIV-1 infection is also associated with other forms of nephropathy, including mesangial hyperplasia. Since HIV-1 gene products are detected in podocytes and other renal cells, it remains uncertain whether podocyte-restricted HIV-1 gene expression can account for the full spectrum of renal lesions involving nonpodocytes. METHODS: To define the role of podocyte-restricted HIV-1 gene expression in the progression of HIVAN, we generated transgenic mice that express nonstructural HIV-1 genes selectively in podocytes. RESULTS: Four of the seven founder mice developed proteinuria and nephropathy. In a subsequently established transgenic line, reverse transcription-polymerase chain reaction (RT-PCR) analysis detected mRNAs for vif, vpr, nef, and spliced forms of tat and rev, but not vpu, in the kidney. In situ hybridization localized HIV-1 RNA to the podocyte. Transgenic mice on FVB/N genetic background exhibited cuboidal morphology of podocytes with reduced extension of primary and foot processes at 2 weeks of age. After 3 weeks of age, these mice developed massive and nonselective proteinuria with damage of podocytes and other glomerular cells and, after 4 weeks of age, collapsing FSGS and microcystic tubular dilatation. In marked contrast, transgenic mice with C57BL/6 genetic background showed either normal renal histology or only mild mesangial expansion without overt podocyte damage. CONCLUSION: The present study demonstrates that podocyte-restricted expression of HIV-1 gene products is sufficient for the development of collapsing glomerulosclerosis in the setting of susceptible genetic background.

AIDS-Associated Nephropathy↗
PubMed2026

The cold case of state transition 7 (stt7) mutants of Chlamydomonas reinhardtii, solved by whole-genome sequencing.

The process of State Transitions (ST) corresponds to an STT7 kinase-driven redistribution of the transmembrane LHCII antenna proteins between Photosystem II (PSII) and Photosystem I (PSI), which results from changes in their phosphorylation state. For the past two decades, two LHCII-kinase mutants, stt7-1 and stt7-9, have been instrumental in the study of STs in Chlamydomonas reinhardtii, the former being a null mutant for the kinase but quasi-sterile in crosses, while the latter, although fertile, has a leaky phenotype. Using long-read sequencing, this study further characterized the genetic lesions of the stt7 mutant strains through whole-genome reconstruction and de novo chromosome assembly. In addition, two new stt7 null mutants were generated, one derived by crosses from the original stt7-1 and one obtained by Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-associated protein 9 (Cas9) technology. This work provides a comprehensive genomic characterization of the original stt7-1 null mutant, revealing extensive chromosomal rearrangements and high levels of aneuploidy, associated with increased cell size and meiotic dysfunction. Reassessment of their physiology and genetic backgrounds highlights the need for caution in interpreting genetic information. We thus produced more reliable null mutants for the LHCII-kinase, amenable to genetic crosses for the study of STs in a variety of genetic backgrounds.

Chlamydomonas reinhardtii↗
PubMed2006

Genetic control of oil content in oilseed rape (Brassica napus L.).

In oilseed rape (Brassica napus L.) like in most oleaginous crops, seed oil content is the main qualitative determinant that confers its economic value to the harvest. Increasing seed oil content is then still an important objective in oilseed rape breeding. In the objective to get better knowledge on the genetic determinism of seed oil content, a genetic study was undertaken in two genetic backgrounds. Two populations of 445 and a 242 doubled haploids (DH) derived from the crosses "Darmor-bzh" x "Yudal" (DY) and "Rapid" x "NSL96/25" (RNSL), respectively, were genotyped and evaluated for oil content in different trials. QTL mapping in the two populations indicate that additive effects are the main factors contributing to variation in oil content. A total of 14 and 10 genomic regions were involved in seed oil content in DY and RNSL populations, respectively, of which five and two were consistently revealed across the three trials performed for each population. Most of the QTL detected were not colocalised to QTL involved in flowering time. Few epistatic QTL involved regions that carry additive QTL in one or the other population. Only one QTL located on linkage group N3 was potentially common to the two populations. The comparisons of the QTL location in this study and in the literature showed that: (i) some of the QTL were more consistently revealed across different genetic backgrounds. The QTL on N3 was revealed in all the studies and the QTL on N1, N8 and N13 were revealed in three studies out of five, (ii) some of the QTL were specific to one genetic background with potentially some original alleles, (iii) some QTL were located in homeologous regions, and (iv) some of the regions carrying QTL for oil content in oilseed rape and in Arabidopsis could be collinear. These results show the possibility to combine favourable alleles at different QTL to increase seed oil content and to use Arabidopsis genomic data to derive markers for oilseed rape QTL and identify candidate genes, as well as the interest to combine information from different segregating populations in order to build a consolidated map of QTL involved in a specific trait.

Agriculture↗
PubMed1995

Endotoxin induced uveitis in the mouse: susceptibility and genetic control.

Endotoxin induced uveitis in the mouse provides a useful animal model for acute anterior uveitis in humans. We have investigated the susceptibility of endotoxin-induced uveitis among various mouse strains, and have examined the relationship between genetic background and the resultant inflammatory response to endotoxin. We studied ten strains with differing major histocompatibility-2 genes, lipopolysaccharide response gene, and strains with mast cell depletion and its sham control. Anterior uveitis was induced by injecting 300 micrograms of Salmonella typhimurium endotoxin into one hind footpad. Mice were then killed 8, 12, 16, 20, 24, 48 and 72 hr after endotoxin injection, and vertical sections of the eyes through the pupil-optic nerve axis were evaluated for ocular inflammation. C3H/HeN mice developed severe uveitis. In contrast, C3H/HeJ mice (lipopolysaccharide response gene-) did not develop uveitis even though it has the same genetic background and shares the same major histocompatibility-2 haplotype with C3H/HeN mice (lipopolysaccharide response gene+). The strain that was mast-cell deficient (W/Wv) developed minimal uveitis; however, W/+ mice, with mast cells, developed more inflammation at 48 and 72 hr after endotoxin injection. C3H.SW and FVB/N mice also developed severe uveitis, and BALB/C, CBA/J, and B10.A developed mild uveitis. In conclusion, there is a wide variation in the magnitude and susceptibility to endotoxin among mouse strains. Multiple factors appear to influence this variability, including non-histocompatibility-2 genetic background, the lipopolysaccharide response gene, and the presence of mast cells.

Animals↗
PubMed2001

Similar target, different effects: late-onset ataxia and spatial learning in prion protein-deficient mouse lines.

Several lines of mice with targeted deletion of the prion protein gene (Prnp) have been produced, some of them appearing phenotypically normal, others developing late-onset ataxia. This has been tentatively attributed to the size of the targeted deletion in the Prnp gene. but a masking role of genetic background could not be excluded. Thus, we have crossed an ataxic mutant line with large deletion of Prnp (Ngsk Prnp0/0) with a knockout line showing only partial deletion of Prnp and no neurological deficits (Zrchl Prnp0/0). A F2 generation was then studied for up to 70 weeks for co-segregation of lesion size and behavioral phenotype, including cognitive and neurological anomalies. These mice were later crossed with a recently generated PrP-deficient line also having a large deletion and late-onset ataxia (Zrch2 Prnp0/0). They underwent similar testing for up to 90 weeks. The ataxic phenotype always co-segregates with large homozygous deletions involving either the Ngsk or the Zrch2 allele, independent of genetic background or sex. Compound heterozygous Zrchl/Ngsk mice or Zrch1/Zrch2 mice showed intermediate neurological phenotypes, suggesting a gene-dosage effect of large deletions. At 12 weeks of age, large deletions were also associated with minor non-cognitive impairments in water maze learning, and hyperactivity in open field and elevated zero maze. These impairments were not predictive for the development of ataxia. Thus, the neurological deficits are closely associated with large deletions, which entail an upregulation of the recently discovered prion Doppel protein (Dpl), while genetic background factors seem to be responsible for shifting the onset of neurological symptoms.

Age of Onset↗
PubMed1997

Genetic control of interleukin 12 responsiveness: implications for disease pathogenesis.

We examined the effect of genetic background on Th1/Th2 development. We discuss data demonstrating that genetic background is an important determinant of interleukin-12 (IL-12) responsiveness and the potential implications for disease progression in murine experimental leishmaniasis. Genetic analysis of the differential control of IL-12 responsiveness led to the identification of a controlling locus on the middle portion of murine chromosome 11. This genetic region (or its human counterpart, 5q31) has been associated with increased disease susceptibilities for several atopic, infectious, and autoimmune disorders. We discuss potential roles for genetic control of IL-12 responsiveness in the development of these diseases.

Animals↗
PubMed1994

Characterization of Star and its interactions with sevenless and EGF receptor during photoreceptor cell development in Drosophila.

Loss-of-function mutations in Star impart a dominant rough eye phenotype and, when homozygous, are embryonic lethal with ventrolateral cuticular defects. We have cloned the Star gene and show that it encodes a novel protein with a putative transmembrane domain. Star transcript is expressed in a dynamic pattern in the embryo including in cells of the ventral midline. In the larval eye disc, Star is expressed first at the morphogenetic furrow, then in the developing R2, R5, and R8 cells as well as in the posterior clusters of the disc in additional R cells. Star interacts with Drosophila EGF receptor in the eye and mosaic analysis of Star in the larval eye disc reveals that homozygous Star patches contain no developing R cells. Taken together with the expression pattern at the morphogenetic furrow, these results demonstrate an early role for Star in photoreceptor development. Additionally, loss-of-function mutations in Star act as suppressors of R7 development in a sensitized genetic background involving the Son of sevenless (Sos) locus, and overexpression of Star enhances R7 development in this genetic background. Based on the genetic interactions with Sos, we suggest that Star also has a later role in photoreceptor development including the recruitment of the R7 cell through the sevenless pathway.

Amino Acid Sequence↗
PubMed1962

New genetically homogeneous background for dystrophic mice and their normal counterparts.

A new type of genetically homogeneous dystrophic and comparable normal mice, from an F(1) hybrid cross between 129/Re-dy and C57BL/6J-dy, is now available as a result of a special breeding program. The clinical manifestations in these F(1) hybrid dystrophics correspond closely with those observed in 129/Re-dydy mice, and they give completely comparable results on a variety of research tests. They are, however, considerably healthier than previously available dystrophics, with a growth rate closer to normal and a greatly increased life-span.

Animals↗