| In general opinion, there are main effect genes and enormous minor effect genes do the supporting to the genetic basis of quantitative traits and heterosis in pig, but the situation is remaining unclear. It is very important to understand the relationship between molecular marker and trait or heterosis for heterosis utilization and marker assistant breeding, by way of using the pig linkage map with high density molecular marker and the technology of molecular markers.The experimental pig populations were composite of two parts: the first including 7 populations: Yorkshire from England (Y, n=35), Landrace from Denmark (L, n=46), Meishan from Jiading County (M, n=55), Yorkshire x Landrace (YL, n=32), Landrace x Yorkshire (LY, n=36), Yorkshire x Meishan (YM, n=82), Meishan x Yorkshire (MY, n=47), for the research of correlations between molecular marker and heterosis or trait; the second for the investigations of QTL mapping, it was a reference family of three generations by mating 3 Yorkshire boars and 8 Meishan sows to produce F1, in which 5 boars and 21 sows had been random mated and 180 F2 individuals produced. The pig populations had been raised in a herd with the same equipment and with the same ordinary food standard, and slaughtered at about 90kg, the phenotypes was recorded for growth traits, carcass traits and meat quality traits. All of the individuals were genotyped of 39 micosatellite markers from SSC4, SSC6, SSC7, SSC8 and SSC13 by interval of 20-30cM, and the genotypes were recorded after PCR, PAGE and Ag-dyed.In this paper, the data have been analyzed as follow: (1) traits and heterosis were described statistical analysis by SAS; (2) genetic diversities in different populations were analyzed for marker genotypes by MSA DISPAN and FSTAT, (3) linkage maps were built for the microsatellite markers by CRIMAP; (4) ANOVA analysis were made between single marker loci and heterosis or traits by SAS; (5) analysis of correlations between individual heterozygosity and heterosis were taken by SAS; (6) QTLs mapped by 1 QTL model for traits; (7) QTLs mapped by 2 QTL model considering no interactions between the two QTLs; (D QTLs mapped by 1 QTL model considering imprinting effects for traits. After above, all of the results were displayed as follow.1. There are some characters of heterosis of 10 traits which have been investigated: (1) homogeneity combination (YL + LY) displays useful heterosis in most of 10 traits; but the heterogeneity combination (YM + MY) displays disbeneficial heterosis in most of traits; (2) most of traits displays no parental effect except minor traits have paternal or maternal effect in YL + LY; but most of traits, displays maternal effect in YM + MY.2. The results of genetic diversity analysis indicated that, the average allele was 4.13 inall of the straightbred and Fl crossbred populations, but it was 3.2 in the F2 reference population; the observed heterozgosity (Ho) and polymorphism information content (PIC) were 0.50 and 0.43 in all of the straightbred and Fl crossbred populations, and it was 0.50 and 0.45 in the F2 reference population; the average informative meioses was 217.4 in the F2 reference population; there were 14 marker loci in linkage disequilibrium in the F2 reference population, which taken 35.9 % of all 39 marker loci.3. The lengths of sex average linkage map, the average marker intervals and the ratio of linkage map length of female to male for SSC4, 6, 7, 8 and 13 were 172.3 cM 24.61 cM and 1.08; 168.7 cM 24.1cM andl.l7 191.7 cM 27.39cM and 0.89; 197.3 cM, 28.19cM and 0.97; 178.3 cM 29.72cM and 0.84, respectively; and the map longer in female than in male for SSC4 and SSC6, but shorter in female than in male for SSC7, SSC8 and SSC13. The orders of marker on the linkage map were the same as on USDA-MARC, but the lengths were longer than that of USDA-MARC.4. For the 10 traits or heterosis which have been investigated, in different Fl and straightbred populations, by the ANOVA analysis between single marker loci and heterosis or traits, we could sort the markers to 3 kinds: very significant marker loci (P = 0.01), significant marker loci (P = 0.05) and insignificant marker loci(P>0.05), by which the loci with different genetic effect suggested that, the performance or heterosis primary based on the effects of main working loci (the effects of very significant marker loci), besides, it was influenced by the enormous loci which just have smaller or minor effect on a special trait as a single locus (the effects of significant marker loci and insignificant marker loci).5. For the heterosis of 10 traits which have been investigated, the very significant marker loci there were difference distinctly between YL + LY and YM + MY, the common very significant marker loci among the two combinations was 0-3: BWT, S0161 (SSC4) SWR1130 (SSC6) and SW1856 (SSC7); WDG, SW1856 (SSC7) and SWR2036 (SSC7);FMR, SW1302(SSC6)and SWR2036(SSC7); LEA, S0161 (SSC4); LMP, SW1302 (SSC6); FMP, SWR1130 (SSC6); SP, SW581(SSC7); BP, SW1841(SSC6); DP SW445 (SSC4) and ABF was zero, and all of above loci were on SSC4, SSC6 and SSC7.6. In Fl populations, according to the very significant marker loci and the insignificant marker loci (the total loci minus very significant marker loci), we could divide the general individual heterozygosity (GH, calculated based on total marker loci) into significant individual heterozygosity (SH, calculated based on very significant marker loci) and insignificant individual heterozygosity (IH, calculated based on the other marker loci), and analyze the correlations of the three kinds of individual heterozygosity against theheterosis of BWI\ WDG and FMR in YL + LY and YM + MY, respectively. The results indicated that the negative correlations existed in YL + LY, and the positive correlations existed in YM + MY; and the results in this paper implicated that the analysis of correlations between heterozygosity and heterosis just displayed surface phenomenon, but not revealed the essential of genetic basis of heterosis, that may be the reason of variance results.7. In this paper, 36 QTLs were detected at 0.05 significant chromosome-wise level, of which 10 at 0.01 significant chromosome-wise level. 6 QTLs were mapped on SSC4, the traits were SIW, WM> RLB> LBFT3, BFTlandLIW; 6 QTLs were mapped on SSC6, the traits were BW> HW> SW, SP, NNS and LGW? 8 QTLs were mapped on SSC7, the traits were SP, LLEA, SW> N^ R^ LMW^ FMPandRLF; 6 QTLs were mapped on SSC8, the traits were ADG3^ SPW> MCV2> LEW, LLEA and MMS2; 10 QTLs were mapped on SSC13, the traits were DLR^ WHC> IMF> LEH> MCV2, SW> SP> FMW, FMP and LW, among the QTL loci, part of results was the same as that of reports, but most of the QTL mapping results were new.8. Results of two QTL with no interaction on one chromosome mapped by 2 QTL model indicated that, there were 2 QTLs on SSC7 for BW, FMP and RLF at SWR2306-SW352 and SW252-SW581 possibly; Another 2 QTLs were detected possibly for SW on SSC7 at SW2155-SW1856 and SWR2306-SW352 ; Maybe there were 2 QTLs for RNS on SSC7 at SW352-SW252 and SW252-SW581, and 2 QTLs for MMS2 on SSC8 at S0098-SW268 and SW1085-SW1980. Furthermore, it was possible existing 2 QTLs for WM and HW on SSC4 and SSC6 respectively.9. Contrast to the ordinary model, results of QTL mapping considering the imprinting effects indicated that, for 37 QTL loci, positions of 10 QTLs changed by 5-110cM, two QTLs changed from insignificant to very significant, 11 QTLs changed from significant to insignificant, 6 QTLs changed from very significant to significant, 1 QTL changed from significant to very significant. The results implicated that imprinting effects influenced on heterosis by work on development of traits.
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