Abstract
Hyphal growth of filamentous fungi requires microtubule-based long-distance motility of early endosomes. Since the discovery of this process in Ustilago maydis, our understanding of its molecular basis and biological function has greatly advanced. Studies in U. maydis and Aspergillus nidulans reveal a complex interplay of the motor proteins kinesin-3 and dynein, which co-operate to support bi-directional motion of early endosomes. Genetic screening has shed light on the molecular mechanisms underpinning motor regulation, revealing Hook protein as general motor adapters on early endosomes. Recently, fascinating insight into unexpected roles for endosome motility has emerged. This includes septin filament formation and cellular distribution of the machinery for protein translation.
Highlights
The endocytic system comprises several compartments that receive cargo from the plasma membrane for processing and recycling back to the cell surface or its degradation in the lysosomes [1]
In temperature-sensitive dynein mutants, retrograde EE motility is blocked and Rab7-positive late endosomes/ vacuoles, stained with the blue dye CMAC (7-Amino-4Chloromethylcoumarin), cluster near the hyphal tip. These results suggest that endosomes mature and fuse to form vacuoles as they move away from the tip [64]
The existence of endocytosis and EEs in fungi was a matter of debate until relatively recently
Summary
The endocytic system comprises several compartments that receive cargo from the plasma membrane for processing and recycling back to the cell surface or its degradation in the lysosomes [1]. Endosomes (EEs) are a central compartment in the endocytic pathway (Figure 1) They bind the small GTPase Rab, which, together with its effectors, controls biogenesis, membrane fusion and microtubule-dependent motility in animal cells [2,3,4,5]. Subsequent studies confirmed a role for this microtubule-dependent motor in delivering chitin synthase-containing secretory vesicles [34], and indicated a role in endocytic uptake of the marker dye Lucifer Yellow [20] This suggests that the accumulation of dynein at plus-ends serves as a ‘buffer stop’ that keeps the organelles on the microtubule track [43] This concept assumes a stochastic interaction of dynein and EEs. additional dynein regulators, such as NudF/Lis1 [45], have been shown to be required for retrograde EE motility [36,39]. As most EE motility occurs along microtubule bundles, consisting of anti-polar oriented microtubules [49], ‘hopping’ causes a change in transport www.sciencedirect.com
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