Finding. The chromatin reader MLLT1, famous as ENL in MLL fusions, is required to keep making B cells. Delete it and marrow progenitors, transitional spleen B cells, and blood B cells fall, in the mouse and in a dish. Il7r, Ebf1, and Pax5 drop. The transcriptional wreckage includes B-development, signaling, DNA replication, and mitochondrial-function sets. Put back wild-type MLLT1 and B cells return. Put back a YEATS mutant that cannot read chromatin or RNA and they do not.
Why this paper matters
Leukemia partners are often unstudied in the tissue they came from. This is the normal-B job. The mitochondrial desk keeps the enrichment term and does not upgrade it to a bioenergetic mechanism.
What they actually measured
Conditional KO, in vitro deletion, targets, GSEA including mitochondrial function, YEATS-mutant rescue failure.
How to read the score
Around 60. Score 60.
What to do with it
If you work on B development or YEATS readers, pull Il7r/Ebf1/Pax5 and the mutant rescue. If you need mitochondria, measure them; they only appear in a gene set. The directional implication is that MLLT1’s reader domain maintains B lymphopoiesis, and one of the broken programs is labeled mitochondrial function.