Mouse anti-Human PI15 monoclonal antibody, clone 4C6

Rice blast, caused by the fungus Magnaporthe oryzae, is the most devastating fungal disease of rice. Mowanggu, a local japonica cultivar in Yunnan Province, China, confers broad-spectrum resistance to this pathogen. To identify the resistance gene(s) in Mowanggu, we obtained an F-2 population and 280 F-8 recombinant inbred lines (RILs) from a cross between Mowanggu and CO39, a highly susceptible indica cultivar. A linkage map with 145 simple sequence repeat (SSR) and single feature polymorphism markers over 12 chromosomes was constructed using the 280 RILs. The resistance evaluation of the F-2 and F-8 populations in both the growth chamber and in a natural rice blast nursery showed that a single dominant gene controls blast resistance in Mowanggu. Moreover, nine quantitative trait loci, which were responsible for different partial resistance components, were mapped on chromosomes 2, 3, 6, 8, 9, and 12, making contributions to the phenotypic variation ranging from 3.03 to 6.18 %. The dominant resistance gene, designated Pi49, was mapped on chromosome 11 with genetic distance of 1.01 and 1.89 cM from SSR markers K10 and K134, respectively. The physical distance between K10 and K134 is about 181 kb in the Nipponbare genome. The Pi49 gene accounted for the major phenotypic variation of disease severity in the growth chamber (where plants were inoculated with single blast isolates) and also accounted for most of the phenotypic variance of disease severity, lesion number, diseased leaf area, and lesion size in the blast nursery. Our study not only identified tightly linked markers for introgression of Pi49 into elite rice cultivars via marker-aided selection but also provides a starting point for map-based cloning of the new resistance gene.

Cranial neural crest cells form the majority of the facial skeleton. However exactly when the pattering information and hence jaw identity is established is not clear. We know that premigratory neural crest cells contain a limited amount of information about the lower jaw but the upper jaw and facial midline are specified later by local tissue interactions. The environmental signals leading to frontonasal identity have been explored by our group in the past. Altering the levels of two signaling pathways (Bone Morphogenetic Protein) and retinoic acid (RA) in the chicken embryo creates a duplicated midline on the side of the upper beak complete with egg tooth in place of maxillary derivatives (Lee et al., 2001). Here we analyze the transcriptome 16 h after bead placement in order to identify potential mediators of the identity change in the maxillary prominence. The gene list included RA, BMP and WNT signaling pathway genes as well as transcription factors expressed in craniofacial development. There was also cross talk between Noggin and RA such that Noggin activated the RA pathway. We also observed expression changes in several poorly characterized genes including the upregulation of Peptidase Inhibitor-15 (PI15). We tested the functional effects of PI15 overexpression with a retroviral misexpression strategy. PI15 virus induced a cleft beak analogous to human cleft lip. We next asked whether PI15 effects were mediated by changes in expression of major clefting genes and genes in the retinoid signaling pathway. Expression of TP63, TBX22, BMP4 and FOXE1, all human clefting genes, were upregulated. In addition, ALDH1A2, ALDH1A3 and RA target, RAR beta were increased while the degradation enzyme CYP26A1 was decreased. Together these changes were consistent with activation of the RA pathway. Furthermore, PI15 retrovirus injected into the face was able to replace RA and synergize with Noggin to induce beak transformations. We conclude that the microarrays have generated a rich dataset containing genes with important roles in facial morphogenesis. Moreover, one of these facial genes, PI15 is a putative clefting gene and is in a positive feedback loop with RA. (C) 2015 Elsevier Inc. All rights reserved.