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  • Journal article
    Bardet P-L, Kolahgar G, Mynett A, Miguel-Aliaga I, Briscoe J, Meier P, Vincent J-Pet al., 2008,

    A fluorescent reporter of caspase activity for live imaging

    , PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 105, Pages: 13901-13905, ISSN: 0027-8424
  • Journal article
    Miguel-Aliaga I, Thor S, Gould AP, 2008,

    Postmitotic specification of <i>Drosophila</i> insulinergic neurons from pioneer neurons

    , PLOS BIOLOGY, Vol: 6, Pages: 538-551, ISSN: 1545-7885
  • Journal article
    Sheldon TJ, Miguel-Aliaga I, Gould AP, Taylor WR, Conklin Det al., 2007,

    A novel family of single VWC-domain proteins in invertebrates

    , FEBS LETTERS, Vol: 581, Pages: 5268-5274, ISSN: 0014-5793
  • Journal article
    Baumgardt M, Miguel-Aliaga I, Karlsson D, Ekman H, Thor Set al., 2007,

    Specification of neuronal identities by feedforward combinatorial coding.

    , PLOS Biology, Vol: 5, ISSN: 1545-7885

    Neuronal specification is often seen as a multistep process: earlier regulators confer broad neuronal identity and are followed by combinatorial codes specifying neuronal properties unique to specific subtypes. However, it is still unclear whether early regulators are re-deployed in subtype-specific combinatorial codes, and whether early patterning events act to restrict the developmental potential of postmitotic cells. Here, we use the differential peptidergic fate of two lineage-related peptidergic neurons in the Drosophila ventral nerve cord to show how, in a feedforward mechanism, earlier determinants become critical players in later combinatorial codes. Amongst the progeny of neuroblast 5-6 are two peptidergic neurons: one expresses FMRFamide and the other one expresses Nplp1 and the dopamine receptor DopR. We show the HLH gene collier functions at three different levels to progressively restrict neuronal identity in the 5-6 lineage. At the final step, collier is the critical combinatorial factor that differentiates two partially overlapping combinatorial codes that define FMRFamide versus Nplp1/DopR identity. Misexpression experiments reveal that both codes can activate neuropeptide gene expression in vast numbers of neurons. Despite their partially overlapping composition, we find that the codes are remarkably specific, with each code activating only the proper neuropeptide gene. These results indicate that a limited number of regulators may constitute a potent combinatorial code that dictates unique neuronal cell fate, and that such codes show a surprising disregard for many global instructive cues.
  • Journal article
    Miguel-Aliaga I, Allan DW, Thor S, 2004,

    Independent roles of the <i>Dachshund</i> and <i>Eyes Absent</i> genes in BMP signaling, axon pathfinding and neuronal specification

    , DEVELOPMENT, Vol: 131, Pages: 5837-5848, ISSN: 0950-1991
  • Journal article
    Miguel-Aliaga I, Thor S, 2004,

    Segment-specific prevention of pioneer neuron apoptosis by cellautonomous, postmitotic Hox gene activity

    , DEVELOPMENT, Vol: 131, Pages: 6093-6105, ISSN: 0950-1991
  • Journal article
    Chan YB, Miguel-Aliaga I, Franks C, Thomas N, Trülzsch B, Sattelle DB, Davies KE, van den Heuvel Met al., 2003,

    Neuromuscular defects in a Drosophila survival motor neuron gene mutant

    , Human Molecular Genetics, Vol: 12, Pages: 1367-1376, ISSN: 0964-6906

    Autosomal recessive spinal muscular atrophy (SMA) is linked to mutations in the survival motor neuron (SMN) gene. The SMN protein has been implicated at several levels of mRNA biogenesis and is expressed ubiquitously. Studies in various model organisms have shown that the loss of function of the SMN gene leads to embryonic lethality. The human contains two genes encoding for SMN protein and in patients one of these is disrupted. It is thought the remaining low levels of protein produced by the second SMN gene do not suffice and result in the observed specific loss of lower motor neurons and muscle wasting. The early lethality in the animal mutants has made it difficult to understand why primarily these tissues are affected. We have isolated a Drosophila smn mutant. The fly alleles contain point mutations in smn similar to those found in SMA patients. We find that zygotic smn mutant animals show abnormal motor behavior and that smn gene activity is required in both neurons and muscle to alleviate this phenotype. Physiological experiments on the fly smn mutants show that excitatory post-synaptic currents are reduced while synaptic motor neuron boutons are disorganized, indicating defects at the neuromuscular junction. Clustering of a neurotransmitter receptor subunit in the muscle at the neuromuscular junction is severely reduced. This new Drosophila model for SMA thus proposes a functional role for SMN at the neuromuscular junction in the generation of neuromuscular defects.
  • Journal article
    Allan DW, St Pierre SE, Miguel-Aliaga I, Thor Set al., 2003,

    Specification of neuropeptide cell identity by the integration of retrograde BMP signaling and a combinatorial transcription factor code

    , CELL, Vol: 113, Pages: 73-86, ISSN: 0092-8674
  • Journal article
    Vargas JD, Culetto E, Ponting CP, Miguel-Aliaga I, Davies KE, Sattelle DBet al., 2002,

    Cloning and developmental expression analysis of <i>ltd-1</i>, the <i>Caenorhabditis elegans</i> homologue of the mouse <i>kyphoscoliosis</i> (<i>ky</i>) gene

    , MECHANISMS OF DEVELOPMENT, Vol: 117, Pages: 289-292, ISSN: 0925-4773
  • Journal article
    Miguel-Aliaga I, Chan YB, Davies KE, van den Heuvel Met al., 2000,

    Disruption of SMN function by ectopic expression of the human SMN gene in <i>Drosophila</i>

    , FEBS LETTERS, Vol: 486, Pages: 99-102, ISSN: 0014-5793

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