Given a question and a context passage, generate the answer having the word or phrase from the context passage. Here, the answer should be a shortest continous span from the passage.

Example Input: Context: Christianson syndrome (CS) is an X-linked neurodevelopmental and neurological disorder characterized in males by core symptoms that include non-verbal status, intellectual disability, epilepsy, truncal ataxia, postnatal microcephaly and hyperkinesis. CS is caused by mutations in the SLC9A6 gene, which encodes a multipass transmembrane sodium (potassium)-hydrogen exchanger 6 (NHE6) protein, functional in early recycling endosomes. The extent and variability of the CS phenotype in female heterozygotes, who presumably express the wild-type and mutant SLC9A6 alleles mosaically as a result of X-chromosome inactivation (XCI), have not yet been systematically characterized. Slc9a6 knockout mice (Slc9a6 KO) were generated by insertion of the bacterial lacZ/-galactosidase (-Gal) reporter into exon 6 of the X-linked gene. Mutant Slc9a6 KO male mice have been shown to develop late endosomal/lysosomal dysfunction associated with glycolipid accumulation in selected neuronal populations and patterned degeneration of Purkinje cells (PCs). In heterozygous female Slc9a6 KO mice, -Gal serves as a transcriptional/XCI reporter and thus facilitates testing of effects of mosaic expression of the mutant allele on penetrance of the abnormal phenotype. Using -Gal, we demonstrated mosaic expression of the mutant Slc9a6 allele and mosaically distributed lysosomal glycolipid accumulation and PC pathology in the brains of heterozygous Slc9a6 KO female mice. At the behavioral level, we showed that heterozygous female mice suffer from visuospatial memory and motor coordination deficits similar to but less severe than those observed in X-chromosome hemizygous mutant males. Our studies in heterozygous Slc9a6 KO female mice provide important clues for understanding the likely phenotypic range of Christianson syndrome among females heterozygous for SLC9A6 mutations and might improve diagnostic practice and genetic counseling by helping to characterize this presumably underappreciated patient/carrier group. 
 Question: Mutation of which gene is implicated in the Christianson syndrome?
Example Output: slc9a6

Example Input: Context: Jack Elgin is the European editor of The Economist, which is based in London, England. Jack has a wife named Maria and three kids named Joanne, Julia, and Andrew. Jack subtly changes the family vacation from a lazy week of Mediterranean fun and sun in Corfu, Greece, to a tour of India, because of a story he has to cover. Maria is not as impressed by this as the kids are. Jack himself envisioned a chance to simultaneously work an easy reporting assignment and spend a little quality time with his family. But on the way to India, the airplane, a 747 owned by AM Air, an American airline, makes an unscheduled stopover in Limassol Cyprus, because of a mechanical problem. After a while of waiting inside the Limassol airport, everyone gets back on the plane -- which is then hijacked by a group of terrorists known as the August 15th Movement, led by a Serbian man named Ivanic Loyvek and his right-hand man Karadan Maldic. The terrorists take a silver briefcase from an diplomatic courier, an older man, and it appears to be an important object of their hijack. And they are demanding $50,000,000 from the US State Department in one hour, or everyone on the airplane will die.The demand is met, and Loyvek and Maldic start releasing the women and children, with the men to go last. But as soon as a front passenger door is opened, the local police begins shooting. Inside the plane, the owner of the briefcase retrieves it, only to be killed the terrorists, who take it again.The flight attendants frantically open the rest of the airplane's doors and start getting passengers out, but the terrorists start killing passengers, leading to an explosion. Maria, Joanne, and Julia get out of the airplane, and then Jack, holding Andrew, gets out -- only to watch Maria, Joanne, and Julia get shot by the terrorists. Jack tries to hide Andrew's face so he can't see. Maria and Joanne are killed, but Julia burns to death while crying for help.Jack and Andrew survive. 15 passengers die, and Loyvek and Maldic, the surviving terrorists, escape, knowing that they now have the $50,000,000. Back in London, a devastated Jack is told that the terrorists were captured, but they were released and deported secretly, with no charges and no arrest, the result of some awfully compromised politics. Jack is understandably enraged that Loyvek and Maldic got off scot-free. While helping Andrew cope, Jack tries all the legal ways to ensure justice for his family, but to no avail.Jack even pays a visit to Henry Davidson, a CIA agent who works at the American Embassy in London. Davidson tells Jack that there's little that can be done. The American and British governments are completely impotent when it comes to going after Loyvek and Maldic. Jack decides he has no choice in the matter but to seek revenge. With the help of his ex-intelligence operative friend Kate Stockton, who is well-schooled in the finer points of international intelligence, Jack becomes a one-man anti-terrorist squadron, searching for Loyvek and Maldich. He finds a warehouse they apparently are using as a headquarters. Breaking in, he finds some papers which he takes, and some weapons. The terrorists return, find a flashlight Jack was using, and begin searching the warehouse. Jack returns upstairs, retrieves a machine pistol and loads it with a magazine. He kills three terrorists before escaping.He later breaks into the home of a friend at MI6 and steals a Walther PPK pistol from his home. He shows up at a theatre and makes a scene at the bar, to be sure he is noticed by the bartender. He then follows one of the terrorists in his taxicab, killing him with that weapon. He returns to the theatre and makes a point of apologizing to the bartender. The next day he goes pheasant hunting with his MI6 contact in case he is tested for gunpowder residue.Dogging Jack's trail is FBI agent Jules Bernard, who's cooperating with Scotland Yard on anti-terrorist activities, and who suspects 
 Question: Who is Jack's wife?
Example Output: maria

Example Input: Context: In eukaryotic cells, there are two sub-pathways of nucleotide excision repair (NER), the global genome (gg) NER and the transcription-coupled repair (TCR). TCR can preferentially remove the bulky DNA lesions located at the transcribed strand of a transcriptional active gene more rapidly than those at the untranscribed strand or overall genomic DNA. This strand-specific repair in a suitable restriction fragment is usually determined by alkaline gel electrophoresis followed by Southern blotting transfer and hybridization with an indirect end-labeled single-stranded probe. Here we describe a new method of TCR assay based on strand-specific-PCR (SS-PCR). Using this method, we have investigated the role of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), a member of the phosphatidylinositol 3-kinase-related protein kinases (PIKK) family, in the TCR pathway of UV-induced DNA damage. Although depletion of DNA-PKcs sensitized HeLa cells to UV radiation, it did not affect the ggNER efficiency of UV-induced cyclobutane pyrimidine dimers (CPD) damage. We postulated that DNA-PKcs may involve in the TCR process. To test this hypothesis, we have firstly developed a novel method of TCR assay based on the strand-specific PCR technology with a set of smart primers, which allows the strand-specific amplification of a restricted gene fragment of UV radiation-damaged genomic DNA in mammalian cells. Using this new method, we confirmed that siRNA-mediated downregulation of Cockayne syndrome B resulted in a deficiency of TCR of the UV-damaged dihydrofolate reductase (DHFR) gene. In addition, DMSO-induced silencing of the c-myc gene led to a decreased TCR efficiency of UV radiation-damaged c-myc gene in HL60 cells. On the basis of the above methodology verification, we found that the depletion of DNA-PKcs mediated by siRNA significantly decreased the TCR capacity of repairing the UV-induced CPDs damage in DHFR gene in HeLa cells, indicating that DNA-PKcs may also be involved in the TCR pathway of DNA damage repair. By means of immunoprecipitation and MALDI-TOF-Mass spectrometric analysis, we have revealed the interaction of DNA-PKcs and cyclin T2, which is a subunit of the human transcription elongation factor (P-TEFb). While the P-TEFb complex can phosphorylate the serine 2 of the carboxyl-terminal domain (CTD) of RNA polymerase II and promote transcription elongation. A new method of TCR assay was developed based the strand-specific-PCR (SS-PCR). Our data suggest that DNA-PKcs plays a role in the TCR pathway of UV-damaged DNA. One possible mechanistic hypothesis is that DNA-PKcs may function through associating with CyclinT2/CDK9 (P-TEFb) to modulate the activity of RNA Pol II, which has already been identified as a key molecule recognizing and initializing TCR. 
 Question: Which gene strand is targeted by transcription-coupled repair (TCR)?
Example Output:
the transcribed strand