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

Example input: In 1582 the united provinces invited francis, duke of anjou to lead them; but after a failed attempt to take antwerp in 1583, the duke left the netherlands again. after the assassination of william of orange (10 july 1584), both henry iii of france and elizabeth i of england declined the offer of sovereignty. however, the latter agreed to turn the united provinces into a protectorate of england (treaty of nonsuch, 1585), and sent the earl of leicester as governor-general. this was unsuccessful and in 1588 the provinces became a confederacy. the union of utrecht is regarded as the foundation of the republic of the seven united provinces, which was not recognized by the spanish empire until the peace of westphalia in 1648.
Example output: In what year did francis, duke of anjou leave the netherlands?
Example explanation: The generated question is perfect. Because the question is based on second sentence of the input passage and its answer is 1583.
Q: Nucleotide excision repair (NER) in eukaryotes is a pathway conserved from yeast to humans that removes many bulky chemical adducts and UV-induced photoproducts from DNA in a relatively error-free manner. In addition to the recognition and excision of DNA damage throughout the genome (GGR), there exists a mechanism, transcription-coupled nucleotide excision repair (TCR), for recognizing some types of DNA damage in the transcribed strand of genes in Escherichia coli, yeast and mammalian cells. An obstacle in the repair of the transcribed strand of active genes is the RNA polymerase complex stalled at sites of DNA damage. The stalled RNA polymerase complex may then mediate recruitment of repair proteins to damage in the transcribed strand. Proteins enabling TCR are the Cockayne syndrome B (CSB) protein in humans and its yeast homologue Rad26. Both CSB and Rad26 belong to the Swi2/Snf2 family of DNA-dependent ATPases, which change DNA accessibility to proteins by altering chromatin structure. To address how Rad26 functions in yeast repair, we used the genetic approach of overexpressing Rad26 and examined phenotypic changes, i.e. changes in NER. We found that repair of both the transcribed and the non-transcribed strands is increased. In addition, overexpression of Rad26 partially bypasses the requirement for Rad7 in GGR, specifically in the repair of non-transcribed sequences. As TCR takes place in very localized regions of DNA (i.e. within genes) in wild-type cells, we propose that overexpression of recombinant Rad26 increases accessibility of the damaged DNA in chromatin for interaction with repair proteins.
A:
Which gene strand is targeted by transcription-coupled repair (TCR)?