Biomedical subjects

Alicia Hidalgo

Publications and source records attributed to Alicia Hidalgo.

4 recordsLinked to original sources

PubMed2004

Coupling glial numbers and axonal patterns.

The control of the rate of cell division enables cells to respond to signals from other cells and this promotes the emergence of order as cell mass increases during growth. Glial cell proliferation is coupled to axon guidance, and the sequential deployment of glial cells in constrained numbers enables the sequential sorting out of axons into appropriate trajectories through time.(1) This is achieved by the neuron-dependent regulation of glial division at the G(1) phase. Early on, Prospero plays a key role controlling the G(1) phase and it enables the glia to proliferate in response to neurons. Later, Prospero maintains subsets of glia in G(1) arrest, retaining mitotic potential, whereas non-Prospero glia terminally differentiate. Only this population of Prospero quiescent precursors can overproliferate when neurons are eliminated, inducing a repair response. It is compelling to investigate whether the vertebrate homologue Prox1 may enable the repair response of vertebrate glia.

Animals↗

PubMed2004

Prospero maintains the mitotic potential of glial precursors enabling them to respond to neurons.

During central nervous system development, glial cells need to be in the correct number and location, at the correct time, to enable axon guidance and neuropile formation. Repair of the injured or diseased central nervous system will require the manipulation of glial precursors, so that the number of glial cells is adjusted to that of neurons, enabling axonal tracts to be rebuilt, remyelinated and functional. Unfortunately, the molecular mechanisms controlling glial precursor proliferative potential are unknown. We show here that glial proliferation is regulated by interactions with axons and that the Drosophila gene prospero is required to maintain the mitotic potential of glia. During growth cone guidance, Prospero positively regulates cycE promoting cell proliferation. Neuronal Vein activates the MAPKinase signalling pathway in the glia with highest Prospero levels, coupling axon extension with glial proliferation. Later on, Prospero maintains glial precursors in an undifferentiated state by activating Notch and antagonising the p27/p21 homologue Dacapo. This enables prospero-expressing cells alone to divide further upon elimination of neurons and to adjust glial number to axons during development.

Animals↗

PubMed2003

The control of cell number during central nervous system development in flies and mice.

Growth is confined within a size that is normal for each species, revealing that somehow an organism 'knows' when this size has been reached. Within a species, growth is also variable, but despite this, proportion and structure are maintained. Perhaps, the key element in the control of size is the control of cell number. Here we review current knowledge on the mechanisms controlling cell number in the nervous system of vertebrates and flies. During growth, clonal expansion is confined, the number of progeny cells is balanced through the control of cell survival and cell proliferation and excess cells are eliminated by apoptosis. Simultaneously, organ architecture emerges and as neurons become active they also influence growth. The interactive control of cell number provides developmental plasticity to nervous system development. Many findings are common between flies and mice, other aspects have been studied more in one organism than the other and there are also aspects that are unique to either organism. Although cell number control has long been studied in the nervous system, analogous mechanisms are likely to operate during the growth of other organs and organisms.

Animals↗

PubMed2002

Interactive nervous system development: control of cell survival in Drosophila.

The non-autonomous control of cell survival has long been thought to be a mechanism of adjusting cell populations in the vertebrate nervous system, enabling connectivity and myelination to produce a functional brain. Despite cellular evidence that analogous mechanisms occur in invertebrates, scepticism has long reigned over whether they operate in model organisms such as Drosophila. This has led to speculation that there are inherent differences between the development and evolution of simple brains and the brains of vertebrates. The great paradox has, until recently, been the absence of molecular evidence of trophic factors in Drosophila. Recent data have finally shown that EGFR (epidermal-growth-factor receptor) ligands function in the Drosophila CNS to maintain glial survival. Trophic interactions are, thus, a general mechanism of nervous system development.

Animals↗