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Actin mesh hinders microtubules

An actin mesh (top) is dismantled (bottom) to allow microtubules to move and cytoplasm to stream in the fly oocyte. ST JOHNSTON/ELSEVIER

Like an iron curtain, a mesh of actin keeps microtubules in place in the fly oocyte, according to Katja Dahlgaard, Daniel St Johnston, and colleagues (University of Cambridge, UK). When the mesh comes down, microtubules are washed into a new orientation by free-flowing cytoplasm.

Microtubule orientation in the fly oocyte points transported mRNAs for polarity-inducing proteins in the right direction. The microtubule array starts off nucleated from the anterior end of the oocyte and extending toward the posterior. At late oogenesis, the array is redistributed to lay flat against the edge of the oocyte. At the same time, the cytoplasm of the oocyte begins to churn like a washing machine.

This rearrangement and churning occurs prematurely in mutants of the actin-associated proteins Cappuccino and Spire, resulting in polarity problems. Dahlgaard was imaging oocytes in an attempt to understand how actin or its regulators control the microtubule network. Since microtubules are so fragile, she was fixing her samples as quickly as possible. Her speed revealed a glimpse of a fleeting actin mesh throughout the oocyte cytoplasm. Stabilization of this mesh prevented microtubule reorganization and streaming.

The actin mesh was missing in the Cappuccino and Spire mutants. It was also dismantled in wild-type flies at late oogenesis, when streaming begins. The authors suggest that the mesh physically hinders streaming, which is probably created by kinesin's tugging of large cellular structures such as organelles. Slow kinesin mutants negated the need for a mesh to prevent premature streaming.

Streaming cytoplasm probably aligns microtubules in the direction of flow and pushes them to the cortex, aligning more kinesin traffic and further bolstering streaming. The mesh might physically block microtubules so they can't turn or reach the cortex. Or it might increase cytoplasmic viscosity, thereby slowing kinesin. And St Johnston has yet another hypothesis. "I favor the idea that the mesh is somehow anchoring organelles as kinesin is trying to move them." To address the issue, he says, "we first need to find what's being transported to generate flow."

Reference:

Dahlgaard, K., et al. 2007. Dev. Cell. 13:539–553.[CrossRef][Medline]

Nicole LeBrasseur

lebrasn{at}rockefeller.edu

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This Article Full Text (PDF, 1119K) PPT slides of all figures Alert me when this article is cited Services Email this article Similar articles in this journal Alert me to new content in the JCB Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by LeBrasseur, N. Search for Related Content PubMed Articles by LeBrasseur, N. Social Bookmarking                            What's this?