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

[Q]: Deletions of the proximal long arm of chromosome 15 (bands 15q11q13) are found in the majority of patients with two distinct genetic disorders, Angelman syndrome (AS) and Prader-Willi syndrome (PWS). The deleted regions in the two syndromes, defined cytogenetically and by using cloned DNA probes, are similar. However, deletions in AS occur on the maternally inherited chromosome 15, and deletions in PWS occur on the paternally derived chromosome 15. This observation has led to the suggestion that one or more genes in this region show differential expression dependent on parental origin (genetic imprinting). No genes of known function have previously been mapped to this region. We show here that the gene encoding the GABAA (gamma-aminobutyric acid) receptor beta 3 subunit maps to the AS/PWS region. Deletion of this gene (GABRB3) was found in AS and PWS patients with interstitial cytogenetic deletions. Evidence of beta 3 gene deletion was also found in an AS patient with an unbalanced 13;15 translocation but not in a PWS patient with an unbalanced 9;15 translocation. The localization of this receptor gene to the AS/PWS region suggests a possible role of the inhibitory neurotransmitter GABA in the pathogenesis of one or both of these syndromes.
[A]: Angelman syndrome is associated with deletion of a part of Chromosome 15 but if the deletion occurs in the paternally inherited chromosome 15, what is the disease?


[Q]: Five or six years ago, I attended a lecture on the science of attention. A professor who conducts research over in the medical school was talking about attention blindness, the basic feature of the human brain that, when we concentrate on one task, causes us to miss just about everything else. Because we can't see what we can't see, our lecturer was determined to catch us in the act. He had us watch a video of six people tossing basketballs back and forth, three in white shirts and three in black, and our task was to keep track only of the tosses among the people in white. The tape rolled, and everyone began counting. Everyone except me. I'm dyslexic , and the moment I saw that tape with the confusing basketball tossers, I knew I wouldn't be able to keep track of their movements, so I let my mind wander. I became curious, though, when about 30 seconds into the tape, a gorilla walked in among the players. She (we later learned a female student was in the gorilla suit) stared at the camera, beat her chest with her fist, and then went away while they continued passing the balls. When the tape stopped, the professor asked how many people had counted at least a dozen basketball tosses. Hands went up all over. He then asked who had counted 13, 14, and congratulated those who'd scored the perfect 15. Then he asked, "And who saw the gorilla?" I raised my hand and was surprised to discover I was the only person at my table and one of only three or four in the large room to do so. He'd set us up, trapping us in our own attention blindness. Yes, there had been a trick, but he wasn't the one who had played it on us. By concentrating so hard on counting, we had managed to miss the gorilla in the midst. Attention blindness is the fundamental organizing principle of the brain, and I believe that it presents us with a great opportunity. My take is different from that of many neuroscientists: Where they see the shortcomings of the individual, I sense an opportunity for cooperation. Fortunately, given the interactive nature of most of our lives in the digital age, we have the tools to control our different forms of attention and take advantage of them. It's not easy to admit that everything we've learned about how to pay attention means that we've been missing everything else. It's not easy for us logical, intelligent, confident types to admit that the very key to our success -- our ability to discover a problem and solve it, an achievement obtained in all those years in school and beyond -- may be exactly what limits us. No one ever told us that our way of seeing left out everything else.
[A]: What's the total number of basketball tosses by the players in white shirts in the video?


[Q]: The Bacillus anthracis toxin genes, cya, lef, and pag, can be viewed as a regulon, in which transcription of all three genes is activated in trans by the same regulatory gene, atxA, in response to the same signal, CO2. In atxA+ strains, toxin gene expression is increased 5- to 20-fold in cells grown in 5% CO2 relative to cells grown in air. CO2-enhanced toxin gene transcription is not observed in atx4-null mutants. Here, we used two independent techniques to obtain evidence for additional CO2-induced atxA-regulated genes. First, total protein preparations from atxA4+ and atxA isolates grown in 5% CO2 and in air were examined by two-dimensional electrophoresis. Comparison of the resulting protein patterns indicated that synthesis of non-toxin proteins is influenced by growth in elevated CO2 and the toxin gene regulator, atxA. Second, we generated random transcriptional lacZ fusions in B. anthracis with transposon Tn917-LTV3. Transposon-insertion libraries were screened for mutants expressing CO2-enhanced atxA-dependent beta-galactosidase activity. DNA sequence analysis of transposon insertion sites in 17 mutants carrying CO2- and atxA-regulated fusions revealed 10 mutants carrying independent insertions on the 185-kb toxin plasmid pXO1 which did not map to the toxin genes. The tcr-lacZ fusion mutants (tcr for toxin coregulated) were Tox+, indicating that these genes may not be involved in anthrax toxin gene activation. Our data indicate a clear association of atxA with CO2-enhanced gene expression in B. anthracis and provide evidence that atxA regulates genes other than the structural genes for the anthrax toxin proteins.
[A]:
Which metabolite activates AtxA?