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Inbred Families (inbred + family)
Selected AbstractsPLASTICITY TO LIGHT CUES AND RESOURCES IN ARABIDOPSIS THALIANA: TESTING FOR ADAPTIVE VALUE AND COSTSEVOLUTION, Issue 6 2000Lisa A. Dorn Abstract Plants shaded by neighbors or overhead foliage experience both a reduction in the ratio of red to far red light (R:FR), a specific cue perceived by phytochrome, and reduced photosynthetically active radiation (PAR), an essential resource. We tested the adaptive value of plasticity to crowding and to the cue and resource components of foliage shade in the annual plant Arabidopsis thaliana by exposing 36 inbred families from four natural populations to four experimental treatments: (1) high density, full sun; (2) low density, full sun; (3) low density, neutral shade; and (4) low density, low R:FR-simulated foliage shade. Genotypic selection analysis within each treatment revealed strong environmental differences in selection on plastic life-history traits. We used specific contrasts to measure plasticity to density and foliage shade, to partition responses to foliage shade into phytochrome-mediated responses to the R:FR cue and responses to PAR, and to test whether plasticity was adaptive (i.e., in the same direction as selection in each environment). Contrary to expectation, we found no evidence for adaptive plasticity to density. However, we observed both adaptive and maladaptive responses to foliage shade. In general, phytochrome-mediated plasticity to the R:FR cue of foliage shade was adaptive and counteracted maladaptive growth responses to reduced PAR. These results support the prediction that active developmental responses to environmental cues are more likely to be adaptive than are passive resource-mediated responses. Multiple regression analysis detected a few costs of adaptive plasticity and adaptive homeostasis, but such costs were infrequent and their expression depended on the environment. Thus, costs of plasticity may occasionally constrain the evolution of adaptive responses to foliage shade in Arabidopsis, but this constraint may differ among environments and is far from ubiquitous. [source] OBSL1 mutations in 3-M syndrome are associated with a modulation of IGFBP2 and IGFBP5 expression levels,HUMAN MUTATION, Issue 1 2010Celine Huber Abstract 3-M syndrome is an autosomal recessive disorder characterized by severe pre- and postnatal growth retardation and minor skeletal changes. We have previously identified CUL7 as a disease-causing gene but we have also provided evidence of genetic heterogeneity in the 3-M syndrome. By homozygosity mapping in two inbred families, we found a second disease locus on chromosome 2q35,36.1 in a 5.2-Mb interval that encompasses 60 genes. To select candidate genes, we performed microarray analysis of cultured skin fibroblast RNA from one patient, looking for genes with altered expression; we found decreased expression of IGFBP2 and increased expression of IGFBP5. However, direct sequencing of these two genes failed to detect any anomaly. We then considered other candidate genes by their function/location and found nine distinct mutations in the OBSL1 gene in 13 families including eight nonsense and one missense mutations. To further understand the links between OBSL1, CUL7, and insulin-like growth factor binding proteins (IGFBPs), we performed real-time quantitative PCR (RT-PCR) analysis for OBSL1, CUL7, IGFBP2, and IGFBP5, using cultured fibroblast RNAs from two patients with distinct OBSL1 mutations (p.F697G; p.H814RfsX15). We found normal CUL7 mRNA levels but abnormal IGFBP2 and IGFBP5 mRNA levels in the two patients, suggesting that OBSL1 modulates the expression of IGFBP proteins. Hum Mutat 30:1,7, 2009. © 2009 Wiley-Liss, Inc. [source] Inbreeding Effects on Hatchery and Growout Performance of Pacific White Shrimp, Penaeus (Litopenaeus) vannameiJOURNAL OF THE WORLD AQUACULTURE SOCIETY, Issue 4 2008Dustin R Moss In animal breeding programs, selection coupled with a narrow genetic base can cause high levels of inbreeding to occur rapidly (in one or two generations). Although the effects of inbreeding have been studied extensively in terrestrial animals and to a lesser extent in aquaculture species, little is known about the effects of inbreeding on penaeid shrimp. The objective of this study was to investigate the effects of inbreeding on hatchery and growout performance of the Pacific white shrimp, Penaeus vannamei. The experiment was conducted over 2 yr, and data from two successive generations (G2 and G3) of inbred (sibling,sibling mating) and outbred families were analyzed. There were 11 inbred and 12 outbred families in G2 and 9 inbred and 10 outbred families in G3. Inbreeding coefficients (F) for outbred and inbred families were 0.00 and 0.25, respectively, for G2 and 0.00 and 0.375, respectively, for G3. Growth rates for outbreds and inbreds were similar in both G2 and G3. Hatch rate for inbred families was 33.1% lower than for outbred families in G2 and 47.1% lower in G3. Inbreeding depression (IBD) (relative change in phenotype per 0.1 increase in F) ± 95% CI for hatch rate was ,12.3 ± 10.1%. Hatchery survival for inbred families was 31.4% lower than for outbred families in G2 and 38.8% lower in G3. IBD for hatchery survival was ,11.0 ± 5.7%. Growout survival was 1.9% lower for inbred families than for outbred families in G2 and 19.6% lower in G3. IBD for growout survival was ,3.8 ± 2.9%. There was also a significant linear relationship between IBD estimates for survival traits and mean outbred survival. At high outbred survival, IBD was low (e.g., growout survival in G2), but IBD appeared to become more severe when outbred survival was lower. This suggests that stress (related to environment and/or life stage) may worsen IBD for survival traits. Results also indicate that moderate to high levels of inbreeding (>10%) should be avoided in commercial shrimp hatcheries because the cumulative effect of IBD on hatch rate and hatchery survival will significantly reduce postlarvae production. Thus, IBD can be significant enough to justify the use of inbreeding as a germplasm protection strategy (under certain scenarios) for genetic improvement programs. [source] Autosomal Recessive Idiopathic Epilepsy in an Inbred Family from Turkey: Identification of a Putative Locus on Chromosome 9q32-33EPILEPSIA, Issue 5 2004Betül Baykan Summary: Purpose: The study describes the clinical features of an inbred family from Turkey with three members affected by seizures and tests possible autosomal recessive (AR) inheritance by means of linkage analysis. Methods: Personal and family history was obtained from each subject, and general physical, neurologic, and EEG examinations were performed. A set of 382 fluorescence-labeled markers was used for the initial genome-wide search. A further set of 83 markers was used to map the locus precisely and to exclude the remaining genome. Results: Twelve individuals from three generations were examined. Two subjects were affected by idiopathic epilepsy, whereas, their brother experienced a single unprovoked generalized seizure. Two siblings affected by idiopathic epilepsy and their unaffected sister showed a photoparoxysmal response to photic stimulation. Nine family members reported migraine. The genome-wide search led to the identification of a unique homozygous, 15.1-cM region shared by subjects with seizures on chromosome 9q32-33 and providing a lod score of 2.9. This locus, however, was not associated with migraine in this pedigree. Conclusions: The study suggests that idiopathic epileptic traits with AR inheritance might be underestimated in the general population and that inbred pedigrees may represent powerful tools for the identification of AR genes. [source] A Novel Early Onset Lethal Form of Catecholaminergic Polymorphic Ventricular Tachycardia Maps to Chromosome 7p14-p22JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2007Ph.D., ZAHURUL A. BHUIYAN M.D. Introduction: Previously, autosomal dominant catecholaminergic polymorphic ventricular tachycardia (CPVT [1]) was mapped to chromosome 1q42,43 with identification of pathogenic mutations in RYR2. Autosomal recessive CPVT (2) was mapped to chromosome 1p13,21, leading to the identification of mutations in CASQ2. In this study, we aimed to elucidate clinical phenotypes of a new variant of CPVT (3) in an inbred Arab family and also delineate the chromosomal location of the gene causing CPVT (3). Methods and Results: In a highly inbred family, clinical symptoms of CPVT appeared early in childhood (7,12 years) and in three of the four cases, the first appearance of symptoms turned into a fatal outcome. Parents of the affected children were first-degree cousins and without any symptoms. Segregation analysis suggested an autosomal recessive inheritance. A genome-wide search using polymorphic DNA markers mapped the disease locus to a 25-Mb interval on chromosome 7p14-p22. A maximal multipoint LOD score of 3.17 was obtained at marker D7S493. Sequencing of putative candidate genes, SP4, NPY, FKBP9, FKBP14, PDE1C, and TBX20, in and around this locus, did not reveal any mutation. Conclusions: We have identified a novel highly malignant autosomal recessive form of CPVT and mapped this disorder to a 25-Mb interval on chromosome 7p14-p22. [source] | |||||||||||||