Inheritance of Ear Tip-Barrenness Trait in Maize

The aim of this paper is to study the inheritance pattern of ear tip-barrenness trait in maize （Zea mays L.）. Ear tipbarrenness trait in maize can be classified into two types, tip-barren and tip-barrenless. Two inbred lines, lx01-3 （tipbarrenless type）, wx04-1 （tip-barren type）, and their F1, F2, BC1, BC2 generations were analyzed on their ear tip-barrenness types. Results showed that F1 was tip-barren type; the ratio of tip-barren type versus tip-barrenless type followed a 12.78： 1 ratio in F2 segregation population and a 2.75：1 ratio in BC1. Z2 test indicated that the trait of ear tip-barrenness type followed an inheritance pattern of 2 duplicate dominant genes. SPSS analysis indicated that the trait of ear tip-barrenness length is of abnormal distribution. Above results mean that： （1） The trait of maize ear tip-barrenness type is controlled by 2 duplicate dominant genes; tip-barren type is dominant over tip-barrenless type; （2） the trait of tip-barrenness length is a quantitative character controlled by polygene with major genes expected.

Genetic Analysis of Grain Yield in a 7×7 Diallel Cross F_2 Population of Wheat(T.Aestivum L.)

In order to obtain genetic information for grain yield, seven genetically diverse wheat cultivars were crossed in an incomplete diallel to study the inheritance of grain yield using F_2 progenies for two years. Significant differences were observed among genotype, year and genotype × year interaction for grain yield, and both general combining ability(GCA) and specific combining ability(SCA) were also highly significant for grain yield, suggesting that the trait was controlled by both additive and non-additive effect. The GCA estimates revealed that the best combiners for grain yield were Yangmai 5 and Ningmai 9. Adequacy tests revealed that data of grain yield was fully adequate for genetic interpretation. Over-dominance genetic effects were important for the expression of grain yield. Grain yield exhibited moderately high value of narrow sense heritability(h_N^2=66.98% and h_N^2=72.37%).

Autosomal dominant coralliform cataract related to a missense mutation of the γD-crystallin gene

Background Congenital cataract is a sight-threatening disease that affects about 1-6 cases per 10000 live births and causes 10%-30% of all blindness in children About 25% of all cases are due to genetic defects We identified autosomal dominant congenital coralliform cataracts-related genetic defect in a four-generation Chinese family Methods Complete ophthalmological examinations were performed prior to lens extraction Lens samples were then studied by electron microscopy Genomic DNA from family members were examined using whole-genomic linkage analysis, with two-point logarithm of odds (LOD) scores calculated using the Linkage program package (version 5 1) Mutation analysis of candidate genes was performed by direct sequencing Finally, a three-dimensional protein model was predicted using Swiss-Model (version 2 0) Results Eleven of the 23 examined individuals had congenital cataracts Ultrastructure studies revealed crystal deposits in the lens, and granules extensively dispersed in transformed lens fiber cells The maximum two-point LOD score, 3 5 at θ=0 1, was obtained for the marker D2S325 Mutation analysis of the γ-crystallin (CRYG) gene cluster identified a mutation (P23T) in exon 2 of γD-crystallin (CRYGD) Protein structure modeling demonstrated that the P23T mutation caused a subtle change on the surface of the γD protein Conclusions The results suggest that the coralliform cataract phenotype is due to a mutated CRYGD gene, and that this sequence change is identical to one reported by Santhiya to be related to another distinct clinical condition, lamellar cataract This study provides evidence that this same genetic defect may be associated with a different phenotype This is the first report identifying the genetic defect associated with an autosomal dominant congenital coralliform cataract

Decreased osteogenic activity and mineralization of alveolar bone cells from a patient with amelogenesis imperfecta and FAM83H 1261G>T mutation

FAM83H mutations lead to autosomal dominant hypocalcified amelogenesis imperfecta(ADHCAI).However,the biological role of FAM83H remains unclear.The present study aimed to characterize the alveolar bone cells isolated from a patient with ADHCAI having the mutation,c.1261G>T,p.E421*,in FAM83H.We showed that FAM83H mutant cells had proliferation ability and morphology similar to the controls.The F-actin staining revealed that FAM83H mutant cells were remained in the earlier stages of cell spreading compared to the controls at 30 min,but their spreading was advanced comparable to the controls at later stages.After osteogenic induction,a significant decrease in mRNA levels of RUNX2 and ALP was observed in FAM83H mutant cells at day 7 compared with day 3 while their expressions were increased in the controls.The OPN levels in FAM83H mutant cells were not significantly changed at day 7 compared to day 3 while the controls showed a significant increase.After 14 days,the mineral deposition of FAM83H mutant cells was slightly lower than that of the controls.In conclusion,we identify that FAM83H bone cells have lower expression of osteogenic marker genes and mineralization while they maintain their morphology,proliferation,and spreading.Consistent with previous studies in the ameloblasts and periodontal ligamental cells,these evidences propose that FAM83H influences osteogenic differentiation across different cell types in oral cavity.