Taken together, multiple mechanisms may operate hierarchically between the NB and the specification of newborn neurons to increase neuron diversity. Knocking down Kr from the NB led to skipping of a single temporal fate during
adPN neurogenesis (Figure 3B). Removing Kr from specific GMCs further revealed that GMC, which normally makes the missing adPN, had precociously adopted the next NVP-AUY922 datasheet temporal fate in the absence of Kr (Figure 3C). These observations indicate that Kr regulates temporal fate transitions in the adPN NB and is continuously required in the GMC to suppress the next temporal fate. Despite no evidence for the involvement of Hb/Pdm/Cas, Kr’s role in delaying fate transition in the Kr-positive GMC suggests an analogous role in an alternate temporal cascade that confers a specific temporal fate from a set of contiguous fates (Figure 4C, Kr part). Furthermore, loss of Kr exerted no detectable effect on the remaining cascade, reminiscent of the chain control in the sequential expression of Hb/Kr/Pdm/Cas. Kr confers the VA7l fate in adPN lineage. Notably, the temporal fate that precedes VA7l fate defines a polyglomerular this website PN with a rather diffuse AL elaboration (Figure S4A). It is challenging to definitely locate the embryonic-born polyglomerular adPN due to colabeling with a large number of uniglomerular siblings. To exclude Hb
as the temporal factor that precedes Kr, we reexamined whether the embryonic-born polyglomerular adPN exists and has properly differentiated in hb mutant NB clones. We used a combination of two sparse GAL4 drivers that collectively label three adPNs, including the embryonic polyglomerular PN plus two earlier-born uniglomerular siblings, to identify NB clones generated near the beginning of the lineage and simultaneously to assess the pre-VA7l polyglomerular PN. We observed the same three adPNs in the wild-type, TCL hb, as well as Kr mutant NB clones ( Figure S4). These results strengthen the conclusion that Kr acts alone without Hb/Pdm/Cas to specify only one middle temporal fate in the protracted adPN lineage. In contrast to Kr defining only one temporal
fate, Chinmo acts in two windows to support eight temporal fates in the adPN lineage. The two windows are separated by only one Chinmo-independent adPN that happens to split two otherwise indistinguishable VM3-targeting adPNs (Figure 2K). Interestingly, the fate transformation of the last two embryonic adPNs (transformed from the VM3[b] and DL4 types to larval-born D type) is similar to the chinmo-elicited fate transformation of larval-born adPNs ( Figures 2K and S2). Chinmo has previously been implicated in governing neuronal temporal identity in the MB lineage and one partially resolved neuronal lineage (Zhu et al., 2006 and Yu et al., 2009). Here, we observed a distinct pattern of Chinmo requirement in the adPN lineage (Figure 2K).
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