TASK DEFINITION: Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.
PROBLEM: Greenwich is on the River, five miles from the middle of London, and its history is two thousand years old. The first English people were fishermen there, and they named the place Greenwich, meaning "green village". Later the English kings and queens lived at Greenwich in their beautiful places. The name of the earliest palace was Placentia. Henry VIII lived there. He knew that England must be strong at sea. So he started two big ship-yards at Greenwich. But trouble was coming to Greenwich. In 1649, a war started in England and for eleven years there was no king. The men who had worked for him at Placentia decided to live the place themselves. They sold all its beautiful things. Finally, the war ended and King Charles II came back. But Placentia was falling down. So King Charles built a new and bigger palace, which is now open to the public. At this time, Charles was worried about losing so many of its ships at sea: their sailors did not know how to tell exactly where they were. So in 1675, Charles made John Flamsteed, the first astronomer in England, try to find the answer. Flamsteed worked in a new building on the high ground in Greenwich Park. From it with a telescope which he made himself, Flamsteed could look all round the sky. And he did, night after night, for twenty years. Carrying on Flamsteed's work a hundred years later, an astronomer called Harrison finally made a clock which told the time at sea, and helped sailors to know where they were. You can see Harrison's clock, still working, in Greenwich's museum of the sea. Because of Flamsteed's work, every country in the world now tells its time by Greenwich Time.

SOLUTION: Who made the first clock which could tell the time at sea?

PROBLEM: 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.

SOLUTION: What is the characteristic domain of histone methyltransferases?

PROBLEM: Somatic mutations in the epidermal growth factor receptor (EGFR) gene are associated with the responses to the tyrosine kinase inhibitors gefitinib and erlotinib in patients with non-small-cell lung cancer (NSCLC). Although various methods for detecting EGFR gene mutations have been developed, they have several disadvantages. We attempted to establish a new method for the detection of EGFR gene mutations with the use of paraffin-embedded samples. The detections of T790M mutations in exon 20 and L858R mutations in exon 21 are based on the principle of allele-specific oligonucleotide polymerase chain reaction (PCR). We also designed PCR primers that enable to detect all types of deletions in exon 19. We assessed the basic performance efficiency of this method, and to confirm its clinical applicability, we performed PCR using DNA extracted from 66 tissue sections that were obtained from patients with NSCLC and embedded in paraffin. The sensitivity of this method for the detection of deletions or mutations was as low as 0.5%. In the 66 subjects whose samples were analyzed, we detected the following deletions and mutations in the EGFR gene: 11 deletions in exon 19, 8 L858R mutations, and 1 double mutation of L858R and T790M. The present method is sensitive and specific for the detection of deletions and mutations in the EGFR gene and is thus suitable for use in laboratory tests.

SOLUTION:
Mutations in which gene determine response to both erlotinib and gefitinib?