@article {68067,
	title = {Hormone-controlled changes in the differentiation state of post-mitotic neurons.},
	journal = {Current Biology},
	volume = {32},
	year = {2022},
	month = {2022 May 23},
	pages = {2341-2348},
	abstract = {<p>While we think of neurons as having a fixed identity, many show spectacular plasticity. Metamorphosis drives massive changes in the fly brain; neurons that persist into adulthood often change in response to the steroid hormone ecdysone. Besides driving remodeling, ecdysone signaling can also alter the differentiation status of neurons. The three sequentially born subtypes of mushroom body (MB) Kenyon cells (γ, followed by α{\textquoteright}/β{\textquoteright}, and finally α/β) serve as a model of temporal fating. γ neurons are also used as a model of remodeling during metamorphosis. As γ neurons are the only functional Kenyon cells in the larval brain, they serve the function of all three adult subtypes. Correspondingly, larval γ neurons have a similar morphology to α{\textquoteright}/β{\textquoteright} and α/β neurons-their axons project dorsally and medially. During metamorphosis, γ neurons remodel to form a single medial projection. Both temporal fate changes and defects in remodeling therefore alter γ-neuron morphology in similar ways. Mamo, a broad-complex, tramtrack, and bric-{\`a}-brac/poxvirus and zinc finger (BTB/POZ)\&nbsp;transcription factor critical for temporal specification of α{\textquoteright}/β{\textquoteright} neurons, was recently described as essential for γ remodeling. In a previous study, we noticed a change in the number of adult Kenyon cells expressing γ-specific markers when mamo was manipulated. These data implied a role for Mamo in γ-neuron fate specification, yet mamo is not expressed in γ neurons until pupariation, well past γ specification. This indicates that mamo has a later role in ensuring that γ neurons express the correct Kenyon cell subtype-specific genes in the adult brain.</p>
},
	issn = {1879-0445},
	doi = {10.1016/j.cub.2022.04.027},
	author = {Lai, Yen-Wei and Miyares, Rosa L and Liu, Ling-Yu and Chu, Sao-Yu and Lee, Tzumin and Yu, Hung-Hsiang}
}
@article {4590,
	title = {Hierarchical deployment of factors regulating temporal fate in a diverse neuronal lineage of the Drosophila central brain.},
	journal = {Neuron},
	volume = {73},
	year = {2012},
	month = {2012 Feb 23},
	pages = {677-84},
	abstract = {<p>The anterodorsal projection neuron lineage of Drosophila melanogaster produces 40 neuronal types in a stereotypic order. Here we take advantage of this complete lineage sequence to examine the role of known temporal fating factors, including Chinmo and the Hb/Kr/Pdm/Cas transcriptional cascade, within this diverse central brain lineage. Kr mutation affects the temporal fate of the neuroblast (NB) itself, causing a single fate to be skipped, whereas Chinmo null only elicits fate transformation of NB progeny without altering cell counts. Notably, Chinmo operates in two separate windows to prevent fate transformation (into the subsequent Chinmo-indenpendent fate) within each window. By contrast, Hb/Pdm/Cas play no detectable role, indicating that Kr either acts outside of the cascade identified in the ventral nerve cord or that redundancy exists at the level of fating factors. Therefore, hierarchical fating mechanisms operate within the lineage to generate neuronal diversity in an unprecedented fashion.</p>
},
	issn = {1097-4199},
	doi = {10.1016/j.neuron.2011.12.018},
	author = {Kao, Chih-Fei and Yu, Hung-Hsiang and He, Yisheng and Kao, Jui-Chun and Lee, Tzumin}
}
