CAD cells form neurites in the absence of MAP1B, MAP2, Tau, STOP and Doublecortin
Chesta, ME; Zampar, GG; Bisig, CG; Purro, SA and Arce, CA.
CIQUIBIC. Dpto. Química Biológica, Fac. Cs. Químicas, UNC
Email: mechesta@fcq.unc.edu.ar
CAD cells proliferate in serum-containing medium and emit neurites in the absence of serum. Its re-addition induces neurites retraction. These cells lack several MAPs (microtubule associated proteins) and their microtubules (MTs) are very dynamic. Here we show that Tiam1 and Dishevelled1 (other MAPs) are present in CAD. Morphological, chemical and functional parameters of these cells are similar to those of normal neurons. Despite of lacking MAPs, neurites elongation rate is similar to that of axons in hippocampus primary cultures, challenging widely accepted concepts about the requirement of MTs stabilization by MAPs for neurite elongation.
We also studied if MTs integrity is involved in neurite development and its retraction by serum re-addition. Nocodazol inhibited development and induced shortening of neurites. When MTs were stabilized with Taxol, subsequent treatment with Nocodazol produced no retraction, but serum re-addition did it. CAD cells lack acetylated tubulin (related to MT stabilization) but Trichostatin A induces its increment. This treatment did not prevent retraction by serum re-addition. Another way to stabilize MTs is depleting cells of ATP with sodium azide, however this drug did not prevent serum retraction either. So, even in the absence of many MAPs, CAD processes can be formed normally and their retraction is not impaired by stabilizing MTs.
