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A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE34123 | GEO | 2011/12/03

SECONDARY ACCESSION(S): PRJNA149875

REPOSITORIES: GEO

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A genome-wide analysis reveals that the Drosophila transcription factor Lola promotes axon growth in part by suppressing expression of the actin nucleation factor Spire.

Project description:BackgroundThe phylogenetically conserved transcription factor Lola is essential for many aspects of axon growth and guidance, synapse formation and neural circuit development in Drosophila. To date it has been difficult, however, to obtain an overall view of Lola functions and mechanisms.ResultsWe use expression microarrays to identify the lola-dependent transcriptome in the Drosophila embryo. We find that lola regulates the expression of a large selection of genes that are known to affect each of several lola-dependent developmental processes. Among other loci, we find lola to be a negative regulator of spire, an actin nucleation factor that has been studied for its essential role in oogenesis. We show that spire is expressed in the nervous system and is required for a known lola-dependent axon guidance decision, growth of ISNb motor axons. We further show that reducing spire gene dosage suppresses this aspect of the lola phenotype, verifying that derepression of spire is an important contributor to the axon stalling phenotype of embryonic motor axons in lola mutants.ConclusionsThese data shed new light on the molecular mechanisms of many lola-dependent processes, and also identify several developmental processes not previously linked to lola that are apt to be regulated by this transcription factor. These data further demonstrate that excessive expression of the actin nucleation factor Spire is as deleterious for axon growth in vivo as is the loss of Spire, thus highlighting the need for a balance in the elementary steps of actin dynamics to achieve effective neuronal morphogenesis.

| S-EPMC3262752 | biostudies-literature

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire

Project description:This SuperSeries is composed of the following subset Series: GSE34121: A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORE76) GSE34122: A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORC4) Refer to individual Series

2011-12-03 | E-GEOD-34123 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORE76)

Project description:Transcriptional profiling of Drosophila embryos comparing lola mutant 10-12 hour after egg lay (AEL) embryos to age-matched control embryos. Mutants are homozygous lola nulls (allele lola_ORE76). Two-condition experiment: lola mutant embryos vs. age-matched control embryos. 7 biological replicates, each sample independently collected and containing RNA from approximately 300 embryos. Mutant and control embryos for each replicate were collected simultaneously. Dye-swaps were performed.

2011-12-03 | E-GEOD-34121 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORC4)

Project description:Transcriptional profiling of Drosophila embryos comparing lola mutant 10-12 hour after egg lay (AEL) embryos to age-matched control embryos. Mutants are homozygous isoform K nulls (allele lola_ORC4). Two-condition experiment: lola mutant embryos vs. age-matched control embryos. 7 biological replicates, each sample independently collected and containing RNA from approximately 300 embryos. Mutant and control embryos for each replicate were collected simultaneously. Dye-swaps were performed.

2011-12-03 | E-GEOD-34122 | biostudies-arrayexpress

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORC4)

2011-12-03 | GSE34122 | GEO

A genome-wide analysis reveals that the Drosophila transcription factor, Lola, promotes axon growth in part by suppressing expression of the actin nucleation factor, Spire (allele lola_ORE76)

2011-12-03 | GSE34121 | GEO

YFR016c/Aip5 is part of an actin nucleation complex in yeast.

Project description:The polarisome comprises a network of proteins that organizes polar growth in yeast and filamentous fungi. The yeast formin Bni1 and the actin nucleation-promoting factor Bud6 are subunits of the polarisome that together catalyze the formation of actin cables below the tip of yeast cells. We identified YFR016c (Aip5) as an interaction partner of Bud6 and the polarisome scaffold Spa2. Yeast cells lacking Aip5 display a reduced number of actin cables. Aip5 binds with its N-terminal region to Spa2 and with its C-terminal region to Bud6. Both interactions collaborate to localize Aip5 at bud tip and neck, and are required to stimulate the formation of actin cables. Our experiments characterize Aip5 as a novel subunit of a complex that regulates the number of actin filaments at sites of polar growth.

| S-EPMC6737964 | biostudies-literature

Myosin 1b promotes axon formation by regulating actin wave propagation and growth cone dynamics.

Project description:Single-headed myosin 1 has been identified in neurons, but its function in these cells is still unclear. We demonstrate that depletion of myosin 1b (Myo1b), inhibition of its motor activity, or its binding to phosphoinositides impairs the formation of the axon, whereas overexpression of Myo1b increases the number of axon-like structures. Myo1b is associated with growth cones and actin waves, two major contributors to neuronal symmetry breaking. We show that Myo1b controls the dynamics of the growth cones and the anterograde propagation of the actin waves. By coupling the membrane to the actin cytoskeleton, Myo1b regulates the size of the actin network as well as the stability and size of filopodia in the growth cones. Our data provide the first evidence that a myosin 1 plays a major role in neuronal symmetry breaking and argue for a mechanical control of the actin cytoskeleton both in actin waves and in the growth cones by this myosin.

| S-EPMC5987710 | biostudies-literature

p53-cofactor JMY is a multifunctional actin nucleation factor.

Project description:Many cellular structures are assembled from networks of actin filaments, and the architecture of these networks depends on the mechanism by which the filaments are formed. Several classes of proteins are known to assemble new filaments, including the Arp2/3 complex, which creates branched filament networks, and Spire, which creates unbranched filaments. We find that JMY, a vertebrate protein first identified as a transcriptional co-activator of p53, combines these two nucleating activities by both activating Arp2/3 and assembling filaments directly using a Spire-like mechanism. Increased levels of JMY expression enhance motility, whereas loss of JMY slows cell migration. When slowly migrating HL-60 cells are differentiated into highly motile neutrophil-like cells, JMY moves from the nucleus to the cytoplasm and is concentrated at the leading edge. Thus, JMY represents a new class of multifunctional actin assembly factor whose activity is regulated, at least in part, by sequestration in the nucleus.

| S-EPMC2763628 | biostudies-literature

cJun promotes CNS axon growth.

Project description:A number of genes regulate regeneration of peripheral axons, but their ability to drive axon growth and regeneration in the central nervous system (CNS) remains largely untested. To address this question we overexpressed eight transcription factors and one small GTPase alone and in pairwise combinations to test whether combinatorial overexpression would have a synergistic impact on CNS neuron neurite growth. The Jun oncogene/signal transducer and activator of transcription 6 (JUN/STAT6) combination increased neurite growth in dissociated cortical neurons and in injured cortical slices. In injured cortical slices, JUN overexpression increased axon growth to a similar extent as JUN and STAT6 together. Interestingly, JUN overexpression was not associated with increased growth associated protein 43 (GAP43) or integrin alpha 7 (ITGA7) expression, though these are predicted transcriptional targets. This study demonstrates that JUN overexpression in cortical neurons stimulates axon growth, but does so independently of changes in expression of genes thought to be critical for JUNs effects on axon growth. We conclude that JUN activity underlies this CNS axonal growth response, and that it is mechanistically distinct from peripheral regeneration responses, in which increases in JUN expression coincide with increases in GAP43 expression.

| S-EPMC4008678 | biostudies-literature

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