Best Selling Books by Heather Collins

Hundreds of Would You Rather questions for teenagers and high schoolers.Would you rather... play on a sports team with your crush, or save them from a burning building?Would you rather... be in your school musical, or play on the basketball team?Would you rather... study abroad or swim with sharks?A great stocking stuffer for ages 13 to 17.Order now!

Hundreds of facts about Big Cats.Lions, tigers, cheetahs, leopards, lynx, snow leopards, jaguars, and cougars.

A book of games for Girl''s Night. (Age 16+)Three sections: Would you rather questions, who''s most likely to questions, and never have I ever.A great stocking stuffer!

"Daddy and Me: Golfing Days" is a heartwarming story about a young boy learning golf from his dad. Through fun lessons, laughter, and special moments, the boy discovers that golf isn''t just about hitting the ball-it''s about patience, fun, and spending time together. A perfect book for families who love sports, outdoor adventures, and father-son bonding!

An innovative coloring book that helps teach kids to draw, and use their imagination.Draw and Color! is a positive, fun, and confidence-building activity for any child.A great birthday gift, Christmas present, and a fun distraction on long car rides.With more than 70 scenes to draw and color, this book will keep them entertained for hundreds of hours.Order now!

999 modern, fun, and clean Would You Rather questions.Keep the kids entertained so they don''t go bananas on a long car ride, or when it''s raining at the cottage.Play in a group, or just the two of you. Great for parent/kid/family bonding.Fun to play at birthday parties while you''re waiting for the pizza.Five Star Reviews for Heather Collins'' Would You Rather Game: ""Bought for 8 year old boy. We have spent hours chatting, and laughing because of this book." -Katie"Kids loved it. My 3rd grader (girl) goes to her she-shed and reads it with her girlfriends. And they giggle and giggle!" - Lovemy3babies"Funny book. Our kids ages 5-10 love this book!" - Brian CareyOrder now!

Fill in the blanks to build your own dad jokes.A fun gift for anyone with a sense of humor.Great for kids on a road trip, or a neat group activity for when it''s raining at the cottage.The perfect Father''s Day, Christmas, or birthday gift.Order now!

Part of the Rainbow Reading range for Primary learners.

When participants were asked where they go to get the most helpful support in solving their child''s behavior problem, the majority of respondents reported that they go to the doctor, family, friends, and the Internet for support: Most found these avenues to be helpful in providing that support.

"The inactivation of the tumor suppressor Retinoblastoma (pRB) is a common tumorigenic event that helps cancer cells evade growth suppression. rbf1 is the functional homologue of pRB in Drosophila and rbf1 mutant eye imaginal discs exhibit cell cycle deregulation as well as a sensitivity to both cell death and differentiation defects. A Polycomb group protein, Posterior sex combs (Psc), was identified in a genetic screen designed to find factors that can specifically induce morphological defects in rbf1 mutant eyes. rbf1 mutations enhanced developmental phenotypes caused by Psc overexpression such as ectopic cell death and disorganized ommatidia. Our genetic analysis revealed that Psc-induced developmental defects were strongly influenced by Caf1p55, a shared component of chromatin-associated complexes including a histone chaperone dCAF-1. The expression levels of dCAF-1 components, CAF1p105 and CAF1p180, increased in rbf1 mutants. The upregulation of dCAF-1 was required for both the hypersensitivity of rbf1 mutant cells to Psc-induced cell death and for the cell death normally observed in rbf1 mutant eye discs. We propose that Caf1p105 and Caf1p180 are important determinants of cell death sensitivity in rbf1 mutant cells and contribute to the genetic interaction between Psc and rbf1.dCAF-1 also played a role in cell death sensitivity in other contexts such as wing discs and pupal eye discs. Reducing dCAF-1 components in eye imaginal discs increased EGFR activity offering a potential mechanism for the role of dCAF-1 in cell death. We postulated that other rbf1 mutant properties could be attributed to dCAF-1 upregulation. First, we demonstrated that the Notch pathway is ectopically activated when rbf1 is mutated and that rbf1 mutant eye discs are sensitive to Notch-induced photoreceptor dedifferentiation. Indeed, dCAF-1 was partly responsible for the rbf1 sensitivity to ectopic Notch. RNA-sequencing on eye discs expressing Caf1p180 RNAi was used to identify dCAF-1-regulated genes with the goal of uncovering the transcriptional targets responsible for the connection between EGFR, Notch and dCAF-1. This approach was unsuccessful in identifying candidate genes in these pathways but uncovered a novel set of genes that is regulated by both dCAF-1 and the E2F repressive complex dREAM. This set of commonly-regulated genes included germline-enriched genes that are not normally expressed in eye discs and have been shown to impact tumorigenesis. The significance of these genes in rbf1 mutant cells, where dCAF-1 is upregulated, remains unknown.Due to the pleiotropic nature of PSC overexpression, it was difficult to elucidate why rbf1 mutant cells are sensitized to PSC overexpression. To address this, we investigated the PSC domains required for PSC-induced phenotypes. Both complex formation and chromatin compaction are required to fully reproduce PSC-induced phenotypes such as loss of Sens, cell death and rough adult eyes. A C-terminal truncation, PSCdelta574-1603, and the homologous region alone, PSC233-552, acted as dominant negative forms of PSC causing hyperproliferation of the eye discs, derepression of a Hox gene Abd-B, and large, transparent larvae. Dominant negative PSC transgenes caused a decrease in PC nuclear localization. Surprisingly, these two dominant negative forms of PSC were not properly localized to the nucleus and were found predominantly in the cytoplasm. Some PSC233-552 entered the nucleus and colocalized with PC. PSC transgenes were examined for their ability to interact with rbf1 mutation. All of the transgenes genetically interacted with the loss of rbf1 to enhance the disorganization of photoreceptors albeit not to the same level as full-length PSC. In contrast, rbf1 mutation only increased the cell death phenotype when PSCdelta1-232 or PSCdeltaRING were expressed. The exact nature of the rbf1 mutant sensitization to PSC overexpression remains undetermined. " --