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

In yeast, the macromolecular complex Set1/COMPASS is capable of methylating H3K4, a posttranslational modification associated with actively transcribed genes. There is only one Set1 in yeast; yet in mammalian cells there are multiple H3K4 methylases, including Set1A/B, forming human COMPASS complexes, and MLL1-4, forming human COMPASS-like complexes. We have shown that Wdr82, which associates with chromatin in a histone H2B ubiquitination-dependent manner, is a specific component of Set1 complexes but not that of MLL1-4 complexes. RNA interference-mediated knockdown of Wdr82 results in a reduction in the H3K4 trimethylation levels, although these cells still possess active MLL complexes. Comprehensive in vitro enzymatic studies with Set1 and MLL complexes demonstrated that the Set1 complex is a more robust H3K4 trimethylase in vitro than the MLL complexes. Given our in vivo and in vitro observations, it appears that the human Set1 complex plays a more widespread role in H3K4 trimethylation than do the MLL complexes in mammalian cells.
Which is the histone residue methylated by MLL1?

Schimke immuno-osseous dysplasia (OMIM 242900) is an uncommon autosomal-recessive multisystem disease caused by mutations in SMARCAL1 (swi/snf-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a-like 1), a gene encoding a putative chromatin remodeling protein. Neurologic manifestations identified to date relate to enhanced atherosclerosis and cerebrovascular disease. Based on a clinical survey, we determined that half of Schimke immuno-osseous dysplasia patients have a small head circumference, and 15% have social, language, motor, or cognitive abnormalities. Postmortem examination of 2 Schimke immuno-osseous dysplasia patients showed low brain weights and subtle brain histologic abnormalities suggestive of perturbed neuron-glial migration such as heterotopia, irregular cortical thickness, incomplete gyral formation, and poor definition of cortical layers. We found that SMARCAL1 is highly expressed in the developing and adult mouse and human brain, including neural precursors and neuronal lineage cells. These observations suggest that SMARCAL1 deficiency may influence brain development and function in addition to its previously recognized effect on cerebral circulation.
Mutations in which gene cause Schimke immune-osseous dysplasia?

This marked the first of four games against potential playoff-bound teams in the Texans, Atlanta Falcons, Buffalo Bills, and Indianapolis Colts. The Browns saw their three-game winning streak end as the Texans' defense and run game dominated the Browns in a 23-7 blowout loss. Texans DE J. J. Watt, who played tight end in high school, scored the 5th offensive TD of his career. The Browns' lone score came in the 2nd quarter. A touchdown from Brian Hoyer to Browns' receiver Andrew Hawkins tied the game at 7 in the second quarter. However, the Texans scored the final 16 points of the contest. Hoyer struggled as he was 20/50 passing for 330 yards, throwing only one touchdown while throwing a 4th quarter interception. It was only the second time this season that the Browns got shut out in the second half of a game, an event that also occurred in their 24-6 loss to the Jaguars. With the loss, the Browns fell out of 1st place in the AFC North and into a tie for 3rd place behind the Bengals and Steelers, who both won that week. Defensive linemen John Hughes and Phil Taylor were lost for the season on IR, and Jordan Cameron missed his 3rd straight game due to a concussion. On November 18, the Browns released RB Ben Tate.

Which player had a 4th quarter interception, Hoyer or Hawkins?