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First published online August 11, 2005
doi: 10.1242/10.1242/dev.01972

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Intrinsic and extrinsic regulators of developmental timing: from miRNAs to nutritional cues

University of Minnesota, Department of Genetics, Cell Biology and Development, 6-160 Jackson Hall, 321 Church St SE, Minneapolis, MN 55455, USA

View larger version (52K): [in a new window]   Fig. 1. Seam cell lineages and expression patterns of selected heterochronic genes. (A) The postembryonic cell division pattern of a generic seam cell (left), with the divisions specific to each larval stage color coded. Horizontal bars indicate the time of cell divisions. The triple horizontal bars at the bottom represent alae, hallmark cuticular ridges that are specific to the adult cuticle. Larval (L) stages are indicated on the left, with ticks denoting the molts. Seam cell lineage patterns for several null (0) mutations are shown on the right, together with that of lin-14 gain-of-function (gf) alleles. The mutant lineages are color coded with respect to the wild-type lineage. (B) The expression patterns of selected heterochronic genes. Arrows indicate positive regulatory interactions and bars indicate negative regulatory interactions (direct interactions are shown in blue). (C-E) L3 molt animals identified by a characteristic just-reflexed gonad indicated by the black arrow in C. The cuticle of L3 molt stage wild-type animals is smooth (D), whereas in lin-14(lf) mutants it contains alae (E), cuticular ridges normally synthesized during the L4 molt. (F,G) L3 stage worms expressing scm:gfp, which marks seam cell nuclei. The nuclear gfp signal has been pseudo-colored green to distinguish it from background autofluorescence. The 11 seam blast cell nuclei in the left mid-body (V cells) are shown in wild type (F). In lin-4 mutants at the same stage, there are only six V cells (G), owing to the omission of the L2 stage proliferative division (blue in A), which is normally executed by five V cells. Scale bars: in C, 5 µm for C-E; in G, 50 µm for F,G. lin-4 mutants are longer than wild type.

View larger version (39K): [in a new window]   Fig. 2. C. elegans lin-4 and let-7 miRNA family members and 3'UTR interactions. (A) Examples of heteroduplexes between lin-4 and two out of seven binding sites in the lin-14 3'UTR and the single binding site in the lin-28 3'UTR (Moss et al., 1997; Wightman et al., 1993). The duplexes are imperfect and overall duplex structure varies because of binding site sequence variations; however, the 5' seed region is usually paired. (B) Representative heteroduplexes demonstrating conservation of let-7-binding sites in the 3'UTRs of lin-41 homologs in worm (Ce), flies (Dm) and zebrafish (Zf) (Pasquinelli et al., 2000; Slack et al., 2000). (C,D) Alignments of let-7 and lin-4 family members. Residues identical to C. elegans let-7 or lin-4 are shown in red. The 5' seed region, which is important for binding-site selection, is underlined. (C) Alignment of the four worm (Ce) let-7 miRNA family members with let-7 genes from Drosophila (Dm) and human (Hs). Only a subset of known human let-7 miRNAs is shown (Lim et al., 2003). (D) Alignment of lin-4 miRNA family members (Ambros et al., 2003; Lim et al., 2003).

View larger version (14K): [in a new window]   Fig. 3. Generic neuroblasts from the Drosophila CNS. The neuroblasts (NBs) divide in a stem-cell like fashion, giving rise to a ganglion mother cell (GMC, G) at each division. The GMCs divide to give rise to neurons (n). Although drawn symmetrically for simplicity, the GMC divisions are often asymmetric, giving rise to neurons of different types. The temporal progression of transcription factor expression in the NB specifies temporal identity in the successive GMCs and is indicated by color coding. Cas, Castor; Hb, Hunchback; Kr, Krüppel.

View larger version (41K): [in a new window]   Fig. 4. Temporal control of neuronal differentiation in the fly eye. (A) Simplified diagram of the InR/Tor pathways. (B) Differentiation in the fly eye disc occurs in a temporal gradient from anterior to posterior, as demonstrated by the expression of differentiation markers (anterior is towards the left). Blue marks early fates, red marks intermediate and yellow indicates expression of late identities. Disruptions in Tor/InR signaling alter this temporal progression. (C,D) Loss-of-function mutations in pten cause the precocious expression of neuronal differentiation markers, including Bar. A pten–/– cell clone, marked by loss of GFP expression (C) and outlined in D, expresses the neuronal transcription factor Bar (red) ahead of the normal differentiation front (D, broken line). Similar precocious expression is caused by overexpression of a PI3K subunit. By contrast, loss of InR, PI3K or Tor activity delays differentiation. See Bateman and McNeill (Bateman and McNeill, 2004) for further details. PI3K, phosphoinositide 3 kinase; PIP2 and PIP3, phosphatidylinositol (4,5)-diphosphate and (3,4,5)-triphosphate, respectively; PTEN, phosphatase and tensin homology; TSC, tuberous sclerosis complex. Reproduced, with permission, from Bateman and McNeill (Bateman and McNeill, 2004).

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