Complete Chloroplast Genome Sequence of an Orchid Model Plant Candidate: Erycina pusilla Apply in Tropical Oncidium Breeding

Oncidium is an important ornamental plant but the study of its functional genomics is difficult. Erycina pusilla is a fast-growing Oncidiinae species. Several characteristics including low chromosome number, small genome size, short growth period, and its ability to complete its life cycle in vitro make E. pusilla a good model candidate and parent for hybridization for orchids. Although genetic information remains limited, systematic molecular analysis of its chloroplast genome might provide useful genetic information. By combining bacterial artificial chromosome (BAC) clones and next-generation sequencing (NGS), the chloroplast (cp) genome of E. pusilla was sequenced accurately, efficiently and economically. The cp genome of E. pusilla shares 89 and 84% similarity with Oncidium Gower Ramsey and Phalanopsis aphrodite, respectively. Comparing these 3 cp genomes, 5 regions have been identified as showing diversity. Using PCR analysis of 19 species belonging to the Epidendroideae subfamily, a conserved deletion was found in the rps15-trnN region of the Cymbidieae tribe. Because commercial Oncidium varieties in Taiwan are limited, identification of potential parents using molecular breeding method has become very important. To demonstrate the relationship between taxonomic position and hybrid compatibility of E. pusilla, 4 DNA regions of 36 tropically adapted Oncidiinae varieties have been analyzed. The results indicated that trnF-ndhJ and trnH-psbA were suitable for phylogenetic analysis. E. pusilla proved to be phylogenetically closer to Rodriguezia and Tolumnia than Oncidium, despite its similar floral appearance to Oncidium. These results indicate the hybrid compatibility of E. pusilla, its cp genome providing important information for Oncidium breeding

Identifi cation of the Tumor Factor of Abnormal Cancer Methylation Enzymes as the Catalytic Subunit of Telomerase

OBJECTIVE The objective was to study the relationship between the tumor factor of cancer MATLT and the catalytic subunit of telomerase. The function of telomerase in the blockade of cell differentiation and in the protection of DNA MT resembles closely the function of the tumor factor of cancer MATLT. Because of this close similarity we made an attempt to examine the possibility that the tumor factor of MATLT might be the catalytic subunit of telomerase. METHODS We used purified MAT isozymes, telomerase antibody, immunoprecipitation, and a selective inhibitor of the tumor factor of MATLT from urine to study the relationship between the tumor factor of MATLT and telomerase.RESULTS We were able to show that the tumor MATLT, but not the liver MATL, was selectively inhibited by the telomerase antibody, and the tumor MATLT, but not the liver MATL, was preferentially immunoprecipitated with the telomerase antibody. The catalytic subunit of telomerase was detectable in the tumor MATLT preparation by immunoblotting, but was undetectable in the liver MATL preparation and the tumor MATL preparation stripped off of the tumor factor. In addition, PP-0.39, which is an effective differentiation inducer purified from urine previously found to selectively antagonize the tumor factor of MATLT, was found in this study to be a potent inhibitor of telomerase. The inhibition of telomerase by PP-0.39 was far more sensitive than the elimination of the tumor factor from MATLT.CONCLUSION All results are consistent with the hypothesis that the tumor factor of MATLT is the catalytic subunit of telomerase. Thus, the blockade of cell diff erentiation by telomerase is mediated through its interaction with MAT to affect methylation enzymes, so that hypomethylation of nucleic acids necessary for the cell to undergo differentiation cannot take place

Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4α. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Group 4, suggest future avenues for rational, targeted therapy