Anna Safley Houston and Early Twentieth Century Collectors

Anna Safley Houston was an eccentric woman from Chattanooga who had a compulsive desire to collect antiques. Houston’s glass collection is one of if not the finest glass collections in the world. Houston had much in common with other great collectors from the early twentieth century such as William Randolph Hearst, Armand Hammer, Bella King and others. Houston did a large amount of traveling, visiting every state along with Canada and Cuba. Houston also established a social and professional network of friend and family who helped her overcome certain difficulties of collecting. In addition, Houston wanted her work to be admired, refusing to sell many pieces of glassware because she was saving them for a museum. Houston differed from other collectors in the barriers she overcame in gathering her collection. Most great collectors from the early twentieth century attended prestigious universities and had made significant achievements in academics. Houston was forced to drop out of middle school to assume family responsibilities when her mother died. Also, collectors often were very wealthy as collecting tended to be quite costly. While Houston was a successful business woman, she was not wealthy. When the Great Depression came, Houston would chose to sell her house instead of selling part of her precious collection. Houston would go on to construct a barn to live in with all of her antiques. The fact that Houston was able to amass one of the greatest collections in the world without being wealthy or highly educated is truly remarkable

Roles of brca2 (fancd1) in Oocyte Nuclear Architecture, Gametogenesis, Gonad Tumors, and Genome Stability in Zebrafish

Mild mutations in BRCA2 (FANCD1) cause Fanconi anemia (FA) when homozygous, while severe mutations cause common cancers including breast, ovarian, and prostate cancers when heterozygous. Here we report a zebrafish brca2 insertional mutant that shares phenotypes with human patients and identifies a novel brca2 function in oogenesis. Experiments showed that mutant embryos and mutant cells in culture experienced genome instability, as do cells in FA patients. In wild-type zebrafish, meiotic cells expressed brca2; and, unexpectedly, transcripts in oocytes localized asymmetrically to the animal pole. In juvenile brca2 mutants, oocytes failed to progress through meiosis, leading to female-to-male sex reversal. Adult mutants became sterile males due to the meiotic arrest of spermatocytes, which then died by apoptosis, followed by neoplastic proliferation of gonad somatic cells that was similar to neoplasia observed in ageing dead end (dnd)-knockdown males, which lack germ cells. The construction of animals doubly mutant for brca2 and the apoptotic gene tp53 (p53) rescued brca2-dependent sex reversal. Double mutants developed oocytes and became sterile females that produced only aberrant embryos and showed elevated risk for invasive ovarian tumors. Oocytes in double-mutant females showed normal localization of brca2 and pou5f1 transcripts to the animal pole and vasa transcripts to the vegetal pole, but had a polarized rather than symmetrical nucleus with the distribution of nucleoli and chromosomes to opposite nuclear poles; this result revealed a novel role for Brca2 in establishing or maintaining oocyte nuclear architecture. Mutating tp53 did not rescue the infertility phenotype in brca2 mutant males, suggesting that brca2 plays an essential role in zebrafish spermatogenesis. Overall, this work verified zebrafish as a model for the role of Brca2 in human disease and uncovered a novel function of Brca2 in vertebrate oocyte nuclear architecture