Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

[EX Q]: We're always looking for well-written reviews of books, music, movies, television shows, websites, video games and other products. When writing a review, concentrate on exactly what you liked or didn't like. Give examples of strengths and weaknesses, be descriptive and provide background information on an author, director, actor or musician, if possible. Find professional reviews in magazines or newspapers and see how reviewers deal with their topic, but be sure to express your own voice in your review. Grammar Hint for Reviews: When describing a book, movie, album or anything else, use the present tense. Book Reviews Discuss an author's technique, strengths and weaknesses instead of focusing on the plot. Does the story flow? Is there a strong sense of character and place? Did you stay up until dawn to finish it? Is it good reading for teenagers? What influence did it have on you and why? If you've read other books by the same author, discuss how this book compares. Movie Reviews Think of the major Oscar categories and consider the performances, music, lighting and setting, etc. Do these work together? Did some hold up while others didn't? If the movie is based on a book, discuss whether one is better than the other and why. If the movie is a remake, compare the film to its original. Remember that a well-written movie review should discuss strengths and weaknesses. Some readers may not have seen a movie yet, so don't give away an exciting scene or the ending! College Reviews Begin by providing an overview of the college, including location, size and a description of the campus and/or dorm life. Think about all aspects of your college visit. What academic, athletic and after-class programs are available? What are the students like? What makes the college different from others? Every school has strengths and weaknesses. Be objective. Consider what the school has to offer and who might enjoy or benefit the most from attending there.
[EX A]: Which aspects should be included in all three reviews?

[EX Q]: Polycomb gene silencing requires histone methyltransferase activity of Polycomb repressive complex 2 (PRC2), which methylates lysine 27 of histone H3. Information on how PRC2 works is limited by lack of structural data on the catalytic subunit, Enhancer of zeste (E(Z)), and the paucity of E(z) mutant alleles that alter its SET domain. Here we analyze missense alleles of Drosophila E(z), selected for molecular study because of their dominant genetic effects. Four missense alleles identify key E(Z) SET domain residues, and a fifth is located in the adjacent CXC domain. Analysis of mutant PRC2 complexes in vitro, and H3-K27 methylation in vivo, shows that each SET domain mutation disrupts PRC2 histone methyltransferase. Based on known SET domain structures, the mutations likely affect either the lysine-substrate binding pocket, the binding site for the adenosylmethionine methyl donor, or a critical tyrosine predicted to interact with the substrate lysine epsilon-amino group. In contrast, the CXC mutant retains catalytic activity, Lys-27 specificity, and trimethylation capacity. Deletion analysis also reveals a functional requirement for a conserved E(Z) domain N-terminal to CXC and SET. These results identify critical SET domain residues needed for PRC2 enzyme function, and they also emphasize functional inputs from outside the SET domain.
[EX A]: What is the characteristic domain of histone methyltransferases?

[EX Q]: One of the major histopathological hallmarks of Alzheimer's disease (AD) is cerebral deposits of extracellular -amyloid peptides. Preclinical studies have pointed to glucagon-like peptide 1 (GLP-1) receptors as a potential novel target in the treatment of AD. GLP-1 receptor agonists, including exendin-4 and liraglutide, have been shown to promote plaque-lowering and mnemonic effects of in a number of experimental models of AD. Transgenic mouse models carrying genetic mutations of amyloid protein precursor (APP) and presenilin-1 (PS1) are commonly used to assess the pharmacodynamics of potential amyloidosis-lowering and pro-cognitive compounds. In this study, effects of long-term liraglutide treatment were therefore determined in two double APP/PS1 transgenic mouse models of Alzheimer's disease carrying different clinical APP/PS1 mutations, i.e. the 'London' (hAPPLon/PS1A246E) and 'Swedish' mutation variant (hAPPSwe/PS1E9) of APP, with co-expression of distinct PS1 variants. Liraglutide was administered in 5 month-old hAPPLon/PS1A246E mice for 3 months (100 or 500 ng/kg/day, s.c.), or 7 month-old hAPPSwe/PS1E9 mice for 5 months (500 ng/kg/day, s.c.). In both models, regional plaque load was quantified throughout the brain using stereological methods. Vehicle-dosed hAPPSwe/PS1E9 mice exhibited considerably higher cerebral plaque load than hAPPLon/PS1A246E control mice. Compared to vehicle-dosed transgenic controls, liraglutide treatment had no effect on the plaque levels in hAPPLon/PS1A246E and hAPPSwe/PS1E9 mice. In conclusion, long-term liraglutide treatment exhibited no effect on cerebral plaque load in two transgenic mouse models of low- and high-grade amyloidosis, which suggests differential sensitivity to long-term liraglutide treatment in various transgenic mouse models mimicking distinct pathological hallmarks of AD.
[EX A]:
Which disease the London mutation involved in?