Temporal Transcription Factors and Their Targets Schedule the End of Neural Proliferation in Drosophila

Maurange, Cédric; Cheng, Louise; Gould, Alex P.

doi:10.1016/j.cell.2008.03.034

Cited by 318 publications

(520 citation statements)

References 59 publications

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“…In addition, some progenitors appear to express a second endogenous burst of the same TTF, as has been observed for Kr and Cas in neuroblasts at late embryonic stages and for Cas (and also Seven up) during larval stages ( Fig. 1C) (Cleary and Doe, 2006;Maurange et al, 2008). In principle, such redeployments within the same progenitor, together with changes in progenitor competence, allow the generation of more neuronal/glial temporal identities than there are progenitor TTFs.…”

Section: A Mechanism Linking Birth Order To Neuronal Fate In Drosophilamentioning

confidence: 58%

Temporal control of neuronal diversity: common regulatory principles in insects and vertebrates?

Jacob

Maurange²,

Gould³

2008

Development

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It is well established in species as diverse as insects and mammals that different neuronal and glial subtypes are born at distinct times during central nervous system development. In Drosophila, there is now compelling evidence that individual multipotent neuroblasts express a sequence of progenitor transcription factors which, in turn, regulates the postmitotic transcription factors that specify neuronal/glial temporal identities. Here, we examine the hypothesis that the regulatory principles underlying this mode of temporal specification are shared between insects and mammals, even if some of the factors themselves are not. We also propose a general model for birth-order-dependent neural specification and suggest some experiments to test its validity.

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Section: A Mechanism Linking Birth Order To Neuronal Fate In Drosophilamentioning

confidence: 58%

Temporal control of neuronal diversity: common regulatory principles in insects and vertebrates?

Jacob

Maurange²,

Gould³

2008

Development

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“…Tissues were fixed and immunostained essentially as described (Maurange et al, 2008). The primary antibodies used were: 1:50 mouse anti-Mira (gift of Fumio Matsuzaki, Riken Center, Japan), 1:1000 rabbit or mouse anti-GFP (Invitrogen), 1:200 rabbit antiHsp60A (gift of Alberto Baena-López, NIMR, UK), 1:200 mouse anticytochrome c (clone 7H8.2C12, Invitrogen) and 1:75 mouse anti-CM1 (Invitrogen).…”

Section: Immunostaining and Clone Countsmentioning

confidence: 99%

A Drosophila model for primary coenzyme Q deficiency and dietary rescue in the developing nervous system

Grant

Saldanha²,

Gould

2010

Disease Models &Amp; Mechanisms

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SUMMARYCoenzyme Q (CoQ) or ubiquinone is a lipid component of the electron transport chain required for ATP generation in mitochondria. Mutations in CoQ biosynthetic genes are associated with rare but severe infantile multisystemic diseases. CoQ itself is a popular over-the-counter dietary supplement that some clinical and rodent studies suggest might be beneficial for neurodegenerative diseases. Here, we identify mutations in the Drosophila qless gene, which encodes an orthologue of the human PDSS1 prenyl transferase that synthesizes the isoprenoid side chain of CoQ. We show that neurons lacking qless activity upregulate markers of mitochondrial stress and undergo caspase-dependent apoptosis. Surprisingly, even though experimental inhibition of caspase activity did not prevent mitochondrial disruption, it was sufficient to rescue the size of neural progenitor clones. This demonstrates that, within the developing larval CNS, qless activity is required primarily for cell survival rather than for cell growth and proliferation. Full rescue of the qless neural phenotype was achieved by dietary supplementation with CoQ4, CoQ9 or CoQ10, indicating that a side chain as short as four isoprenoid units can provide in vivo activity. Together, these findings show that Drosophila qless provides a useful model for studying the neural effects of CoQ deficiency and dietary supplementation.A Drosophila model for primary coenzyme Q deficiency and dietary rescue in the developing nervous system mutations, 109 and 264, were isolated in a mosaic screen for genes regulating the size of neural progenitor (neuroblast) clones in the larval Drosophila CNS. Both mutations are embryonic-lethal, and were mapped on the right arm of chromosome 3 by failure to complement molecularly defined deficiencies and a lethal EP element inserted into a previously uncharacterized gene, CG31005 ( Fig. 1A; supplementary material Fig. S1A). The predicted protein product of CG31005 (AAF57135) matches that encoded by human PDSS1 (AAH49211) with a BLASTP E-value of 2ϫ10 -102 . On this basis, and in light of later CoQ rescue studies, we subsequently refer to the CG31005 gene as qless. Sequencing revealed that the qless 109 mutation is a G to A swap at position 1354 of the predicted transcript (CG31005-RA), corresponding to a S215N mutation in the predicted Qless protein (CG31005-PA) ( Fig. 1A; supplementary material Fig. S1B). S215 is located ten amino acids C-terminal to the first of the two predicted aspartate-rich DDxxD sites that mediate substrate binding and catalysis by prenyl transferases (Song and Poulter, 1994). Alignments of PDSS1-related prenyl transferases in a wide variety of different organisms shows that position 215 is highly conserved, with either a serine or threonine occupying this position (Fig. 1B). A protein structural model of the region around the first DDxxD motif predicts that the S215N mutation disrupts hydrogen bonding of residue 215 to the N217 side chain, instead resulting in inappropriate hydrogen bonding to Y148 in the N-terminus...

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“…Firstly, NBs are SCs that operate exclusively during development. Unlike adult SCs that ensure homoestasis through the lifetime of the individual, NBs are programmed to disappear once neurogenesis is completed and are not immortal (Truman and Bate, 1988;Ito and Hotta, 1992;Maurange et al, 2008). Secondly, whereas asymmetric NB division is self-renewing, in the sense that one of the daughters retains NB identity and will continue the programme of asymmetric mitoses, self-renewal might not be complete and daughter NBs might be more restricted than their mother NBs in terms of the cell types that they can generate.…”

Section: Drosophila Nbs As Sc Modelsmentioning

confidence: 99%

Drosophila asymmetric division, polarity and cancer

Januschke

González

2008

Oncogene

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Temporal Transcription Factors and Their Targets Schedule the End of Neural Proliferation in Drosophila

Cited by 318 publications

References 59 publications

Temporal control of neuronal diversity: common regulatory principles in insects and vertebrates?

Temporal control of neuronal diversity: common regulatory principles in insects and vertebrates?

A Drosophila model for primary coenzyme Q deficiency and dietary rescue in the developing nervous system

Drosophila asymmetric division, polarity and cancer

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