6.22.2006

Endosomal Transport in Fungi

The recent paper by JH Lenz et al. describes the mechanism for early endosome trafficking in Ustilago maydis, a pathogenic fungus.

A dynein loading zone for reterograde endosome motility at microtubule plus ends
JH Lenz, I Schuchardt, A Straube and G Steinberg
The EMBO Journal (2006) 25, 2275–2286



The trafficking they are concerned with is that to the hypha tip because polarized growth of the fungus in this area is an important factor controlling its ability to invade the host cell. Not surprisingly the endosomal trafficking is microtubule dependent and occurs via dynein/kinesin cooperation. The take-home message is that kinesin3 carries early endosomes to the hyphal apex where they can contribute to cell expansion before being carried reterogradly by dynein. They find that when they knock out kin3 the hypa are smaller and the early endosomes cluster near the nucleus. This is not surprising given that they use the +TIP EB1 to show that almost 90% of MTs are oriented with their plus end toward the hyphoid tip. Conversely if dynein is knocked out (conditionally) the early endosomes cluster at the hyphoid tip/MT plus-ends. Probably the nicest piece of data in the paper is the microscopy showing that early endosomes move toward the regions of concentrated dynein before reve rsing directions. I’ve taken their Figure 3E (left) where dynein is in green and the early endosomes are in red and you can see the red migrate into the green, then turn yellow and move in the opposite direction. They take their studies a step further and address the question of how dynein is itself regulated during this process. They find that depleting lis1 causes dynein to accumulate at the hyphal tip while depleting dynactin reduces dynein at the tip. Finally they show that kin1 transports dynein/dynactin to the hyphoid tip by showing that knocking out kin1 blocks their accumulation. They go the extra mile and show that dynein does not colocalize with early endosomes moving to the tip and additionally show that the early endosomes still accumulate in the absence of dynein. This data together supports the following model taken from their paper. Inactive dynein is carried to the hypoid tip/MT plus end by kin1. Early endosomes are then transported to the tip at which time lis1 is activated by a yet undetermined mechanism. Lis1 then stimulates dynein dependent reterograde transport of the endosomes for recycling.

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