Plasticity-related gene 3 promotes neurite shaft protrusion.

Tanja Velmans, Arne Battefeld, Beate Geist, Anna Soriguera Farrés, Ulf Strauss, Anja U Bräuer
BMC Neuroscience. 2013-01-01; 14(1): 36
DOI: 10.1186/1471-2202-14-36

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1. BMC Neurosci. 2013 Mar 19;14:36. doi: 10.1186/1471-2202-14-36.

Plasticity-related gene 3 promotes neurite shaft protrusion.

Velmans T(1), Battefeld A, Geist B, Farrés AS, Strauss U, Bräuer AU.

Author information:
(1)Institute of Cell Biology and Neurobiology, Center for Anatomy,
Charité-Universitätsmedizin Berlin, Berlin, Germany.

BACKGROUND: Recently, we and others proposed plasticity-related gene 3 (PRG3) as
a novel molecule in neuritogenesis based on PRG3 overexpression experiments in
neuronal and non-neuronal cell lines. However, direct information on PRG3 effects
in neuronal development and, in particular, its putative spatio-temporal
distribution and conditions of action, is sparse.
RESULTS: We demonstrate here that PRG3 induces filopodia formation in HEK293
cells depending on its N-glycosylation status. The PRG3 protein was strongly
expressed during mouse brain development in vivo from embryonic day 16 to
postnatal day 5 (E16 – P5). From P5 on, expression declined. Furthermore, in
early, not yet polarized hippocampal cultured neurons, PRG3 was expressed along
the neurite shaft. Knock-down of PRG3 in these neurons led to a decreased number
of neurites. This phenotype is rescued by expression of an shRNA-resistant PRG3
construct in PRG3 knock-down neurons. After polarization, endogenous PRG3
expression shifted mainly to axons, specifically to the plasma membrane along the
neurite shaft. These PRG3 pattern changes appeared temporally and spatially
related to ongoing synaptogenesis. Therefore we tested (i) whether dendritic PRG3
re-enhancement influences synaptic currents and (ii) whether synaptic inputs
contribute to the PRG3 shift. Our results rendered both scenarios unlikely: (i)
PRG3 over-expression had no influence on miniature excitatory postsynaptic
currents (mEPSC) and (ii) blocking of incoming signals did not alter PRG3
distribution dynamics. In addition, PRG3 levels did not interfere with intrinsic
neuronal properties.
CONCLUSION: Taken together, our data indicate that endogenous PRG3 promotes
neurite shaft protrusion and therefore contributes to regulating filopodia
formation in immature neurons. PRG3 expression in more mature neurons, however,
is predominantly localized in the axon. Changes in PRG3 levels did not influence
intrinsic or synaptic neuronal properties.

DOI: 10.1186/1471-2202-14-36
PMCID: PMC3623789
PMID: 23506325 [Indexed for MEDLINE]

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