High impact information on Hybrid Vigor

• Molecular basis for heterosis for myelin basic protein content in mice [1].
• We therefore believe that heterosis for brain MBP content in the F1 hybrid may be regulated at the transcriptional or post-transcriptional level [1].
• However, Esr2(+/-) mice do develop more severe clinical disease with an earlier onset indicating that heterosis at Esr2 plays a significant role in regulating EAE in males [2].
• We propose that heterosis provides a mechanism to compensate for UCP1 deficiency [3].
• Specificity controls eliminate the possibility that the differential uptake is due to Fc receptor binding or undefined effects of hybrid vigor [4].

Biological context of Hybrid Vigor

• Heterozygous combinations of members of the same group are intermediate in phenotype compared to the respective homozygotes, whereas heterozygotes of Ax alleles from different groups exhibit negative heterosis, being much less viable and more extremely mutant than either homozygote [5].
• No heterosis or maternal effects were detected in jejunal glucose active transport and active glucose uptake [6].
• For subjects 55 to 70 years of age in Group 1, cholesterol levels were significantly greater in the LS heterozygotes than either LL or SS homozygotes, indicating a heterosis effect (P </= 0.0001) [7].
• While the OLETF allele corresponds with increased glucose levels as expected for Nidd12 and 14/of, the Nidd13/of exhibits heterosis: heterozygotes showing significantly higher glucose levels than OLETF or F344 homozygotes [8].
• A slightly positive association of DRD2 TaqI A1 genotypes with alcoholism was observed, by standard and molecular heterosis approaches [9].

Anatomical context of Hybrid Vigor

• DOPAC showed significant heterosis for all lines only in the optic tectum, and DA showed little heterosis specific to any line, cross, or brain area [10].

Associations of Hybrid Vigor with chemical compounds

• The results for both the DRD1 and DRD2 genes, which have opposing effects on cyclic AMP, were consistent with negative and positive heterosis, respectively [11].
• It was concluded that multilocus probe DFP of pooled DNA samples show promise as predictors of heterosis [12].
• F1 hybrids of crosses between two widely studied wild-type strains, N2 (var. Bristol) and Berg BO (var. Bergerac), were examined for rate of development, hermaphrodite fertility, and behavior; there was no heterosis for these life history traits [13].
• Analysis of the whole brain for several myelin-associated constituents such as GM1 ganglioside, 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase), 5'-nucleotidase, and carbonic anhydrase indicated that heterosis exists for these components [14].
• Similarity indices between different parental combinations, calculated based on seed esterase polymorphism, showed a significant negative correlation (r = -0.479, P = 0.05) with heterosis for carotenoid content [15].

Gene context of Hybrid Vigor

• The possible role of HUMMLC2B and its relation to porcine heterosis are discussed [16].
• The positive heterosis effects with respect to nicotine addiction and personality support the idea that the TPH1 gene exerts pleiotropic effects [17].
• With one exception, heterosis was not an important source of variation for shank width or shank depth and there was a low level of heterosis for shank length [18].
• Heterosis was 8.2% for ADG [19].
• Heterosis percentages were significant for AVBF (7.2%; P less than .01), BF10 (8.8%; P less than .01), DRS% (1.5%; P less than .01), ADG (11.5%; P less than .01), DFC (10.2%; P less than .01), LNGN (10.6%; P less than .01), and LNEF (6.0%; P less than .05) [20].

Analytical, diagnostic and therapeutic context of Hybrid Vigor

• Uterine heterosis on body size was smaller than progeny heterosis, and both progeny and uterine heterosis persisted in adult mice [21].

References