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Targeted disruption of Ca(2+)-calmodulin signaling in Drosophila growth cones leads to stalls in axon extension and errors in axon guidance.

Abstract：

:Ca(2+)-calmodulin (CaM) function was selectively disrupted in a specific subset of growth cones in transgenic Drosophila embryos in which a specific enhancer element drives the expression of the kinesin motor domain fused to a CaM antagonist peptide (kinesin-antagonist or KA, which blocks CaM binding to target proteins) or CaM itself (kinesin-CaM or KC, which acts as a Ca(2+)-binding protein). In both KA and KC mutant embryos, specific growth cones exhibit dosage-dependent stalls in axon extension and errors in axon guidance, including both defects in fasciculation and abnormal crossings of the midline. These results demonstrate an in vivo function for Ca(2+)-CaM signaling in growth cone extension and guidance and suggest that Ca(2+)-CaM may in part regulate specific growth cone decisions, including when to defasciculate and whether or not to cross the midline.

journal_name

Neuron

journal_title

Neuron

authors

VanBerkum MF,Goodman CS

doi

10.1016/0896-6273(95)90239-2

subject

Has Abstract

pub_date

1995-01-01 00:00:00

pages

43-56

issue

1

eissn

0896-6273

issn

1097-4199

pii

0896-6273(95)90239-2

journal_volume

14

pub_type

杂志文章

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