A comparative study of dietary fiber content, In vitro starch digestibility and cooking quality characteristics of pigmented and non-pigmented traditional and improved rice (Oryza sativa L.).

Thirty-two traditional and newly improved pigmented and non-pigmented rice varieties were evaluated for their eating and cooking quality and dietary fiber (DF) content. Seasonal variability of DF content, in-vitro starch digestion rate (DR) and expected glycemic index (eGI) were evaluated using selected representative samples. Rice varieties were categorized either high or intermediate amylose content but with hard, medium or soft gel consistency. Average insoluble dietary fiber (IDF) and soluble dietary fiber (SDF) content ranged between 1.13-6.76% and 0.03-1.00%, respectively. Pigmented rice reported significantly higher IDF content compared to non-pigmented rice and also showed a significant statistical correlation (r > 0.56, P < 0.01) between IDF and pigmentation. There was no seasonal variation observed in rice DF content between two cropping seasons. Pigmented rice varieties showed significantly lower (P < 0.05) starch digestibility and glycemic index values (DR:58.8-66.5; eGI:71.9-76.2) than non-pigmented rice (DR:69.1-71.5; eGI:77.6-79.0). Pigmented rice showed significantly higher negative correlation (r > -0.68, P < 0.01) with DR.

A novel quantitative trait locus for Fusarium head blight resistance in chromosome 7A of wheat.

A Chinese Spring-Sumai 3 chromosome 7A disomic substitution line (CS-Sumai 3-7ADSL) was reported to have a high level of Fusarium head blight (FHB) resistance for symptom spread within a spike (Type II) and low deoxynivalenol accumulation in infected kernels (Type III), but a quantitative trait locus (QTL) on chromosome 7A has never been identified from this source. To characterize QTL on chromosome 7A, we developed 191 7A chromosome recombinant inbred lines (7ACRIL) from a cross between Chinese Spring and CS-Sumai 3-7ADSL and evaluated both types of resistance in three greenhouse experiments. Two major QTL with Sumai 3 origin, conditioning both Type II and III resistance, were mapped in the short arm of chromosomes 3B (3BS) and near the centromere of chromosome 7A (7AC). The 3BS QTL corresponds to previously reported Fhb1 from Sumai 3, whereas 7AC QTL, designated as Fhb7AC, is a novel QTL identified from CS-Sumai 3-7ADSL in this study. Fhb7AC explains 22% phenotypic variation for Type II and 24% for Type III resistance. Marker Xwmc17 is the closest marker to Fhb7AC for both types of resistance. Fhb1 and Fhb7AC were additive, and together explained 56% variation for Type II and 41% for Type III resistance and resulted in 66% reduction in FHB severity and 84% reduction in deoxynivalenol (DON) content. Haplotype analysis of Sumai 3 parents revealed that Fhb7AC originated from Funo, an Italian cultivar. Fhb7AC has the potential to be used in improving wheat cultivars for both types of resistance.

A human YAC transgene rescues craniofacial and neural tube development in PDGFRalpha knockout mice and uncovers a role for PDGFRalpha in prenatal lung growth.

The platelet-derived growth factor alpha-receptor (PDGFRalpha) plays a vital role in the development of vertebrate embryos, since mice lacking PDGFRalpha die in mid-gestation. PDGFRalpha is expressed in several types of migratory progenitor cells in the embryo including cranial neural crest cells, lung smooth muscle progenitors and oligodendrocyte progenitors. To study PDGFRalpha gene regulation and function during development, we generated transgenic mice by pronuclear injection of a 380 kb yeast artificial chromosome (YAC) containing the human PDGFRalpha gene. The YAC transgene was expressed in neural crest cells, rescued the profound craniofacial abnormalities and spina bifida observed in PDGFRalpha knockout mice and prolonged survival until birth. The ultimate cause of death was respiratory failure due to a defect in lung growth, stemming from failure of the transgene to be expressed correctly in lung smooth muscle progenitors. However, the YAC transgene was expressed faithfully in oligodendrocyte progenitors, which was not previously observed with plasmid-based transgenes containing only upstream PDGFRalpha control sequences. Our data illustrate the complexity of PDGFRalpha genetic control, provide clues to the location of critical regulatory elements and reveal a requirement for PDGF signalling in prenatal lung growth, which is distinct from the known requirement in postnatal alveogenesis. In addition, we found that the YAC transgene did not prolong survival of Patch mutant mice, indicating that genetic defects outside the PDGFRalpha locus contribute to the early embryonic lethality of Patch mice.