Although the methylation activity of Trx was required for maintaining the type II neuroblast functional identity, removing trx function did not alter the global H3K4 methylation.
Thus, we propose that in addition to maintaining the type II neuroblast functional identity, Trx also functions to promote INP identity specification through pnt.
Thus, it is formally possible that multiple isoforoms of Pnt or a yet unknown mechanism function to maintain a type II neuroblast functional identity.
If Trx maintains a type II neuroblast functional identity by regulating btd transcription, removing btd function should trigger type II neuroblasts to adopt a type I neuroblast functional identity.
Lastly, additional transcription factors might function in parallel with Btd to regulate the functional identity of a type II neuroblast.
We initially hypothesized that Pnt might function in parallel with Btd to maintain the functional identity of a type II neuroblast.
Together, these data strongly support our hypothesis that btd is an excellent candidate for functioning downstream of trx to maintain the type II neuroblast functional identity.
However, the physiological function of PntP1 in the maintenance of a type II neuroblast functional identity remains unclear.
The phenotypic covariance between two individuals given their diploid genotypes is expressed in terms of functional identity states.
It is poorly understood, however, whether these two disturbances interact with the functional identity of recipient native plants to drive community change.
We used a combined optogenetic-electrophysiological strategy to determine the functional identity of entorhinal cells with output to the place-cell population in the hippocampus.
