Extremes of lineage plasticity in the drosophila brain

Suewei Lin, Elizabeth C. Marin, Ching Po Yang, Chih Fei Kao, Bettye A. Apenteng, Yaling Huang, Michael B. O'Connor, James W. Truman, Tzumin Lee

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

An often-overlooked aspect of neural plasticity is the plasticity of neuronal composition, in which the numbers of neurons of particular classes are altered in response to environment and experience. The Drosophila brain features several well-characterized lineages in which a single neuroblast gives rise to multiple neuronal classes in a stereotyped sequence during development [1]. We find that in the intrinsic mushroom body neuron lineage, the numbers for each class are highly plastic, depending on the timing of temporal fate transitions and the rate of neuroblast proliferation. For example, mushroom body neuroblast cycling can continue under starvation conditions, uncoupled from temporal fate transitions that depend on extrinsic cues reflecting organismal growth and development. In contrast, the proliferation rates of antennal lobe lineages are closely associated with organismal development, and their temporal fate changes appear to be cell cycle-dependent, such that the same numbers and types of uniglomerular projection neurons innervate the antennal lobe following various perturbations. We propose that this surprising difference in plasticity for these brain lineages is adaptive, given their respective roles as parallel processors versus discrete carriers of olfactory information.

Original languageEnglish (US)
Pages (from-to)1908-1913
Number of pages6
JournalCurrent Biology
Volume23
Issue number19
DOIs
StatePublished - Oct 7 2013

Bibliographical note

Funding Information:
We thank Chihiro Hama at Kyoto Sangyo University for sle 057 , Ulrike Heberlein at HHMI Janelia Farm Research Campus for the UAS-InR flies, Julie Simpson at HHMI Janelia Farm Research Campus for the nSyb-GAL4 flies, Carl Thummel at the University of Utah for the AD4.4 antibody, and members of the Marin and Lee groups for thoughtful comments on the manuscript. J.W.T. was funded by the Howard Hughes Medical Institute and a grant from the National Institutes of Health (NS13079). T.L. was funded by the Howard Hughes Medical Institute and a grant from the National Institutes of Health (MH080739).

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