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Microtubule Destablizers Control Axon and Dendrite The Pennsylvania State University The Graduate School Eberly College of Science MICROTUBULE DESTABLIZERS CONTROL AXON AND DENDRITE DISASSEMBLY AFTER INJURY AND DURING PRUNING A Dissertation in Biochemistry, Microbiology, and Molecular Biology by Juan Tao © 2014 Juan Tao Submitted in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy December 2014 ii The dissertation of Juan Tao was reviewed and approved* by the following: Melissa M. Rolls Associate Professor of Biochemistry and Molecular Biology Dissertation Advisor Chair of Committee Lorraine Santy Associate Professor of Biochemistry and Molecular Biology Zhi-Chun Lai Professor of Biology Professor of Biochemistry and Molecular Biology Richard W. Ordway Associate Professor of Biology Scott Selleck Professor of Biochemistry and Molecular Biology Head of the Department of Biochemistry and Molecular Biology *Signatures are on file in the Graduate School iii Abstract A neuron extends one axon and several dendrites far from its cell body, leaving these extremely thin processes subject to various insults, including physical damages, strokes, and neurodegenerative diseases during aging. Axon degeneration after injury, called Wallerian degeneration, was discovered in mice two decades ago, yet few molecular mechanisms that control the degeneration process have been identified. To study injury-induced and developmental degeneration, our lab used Drosophila dendritic arborization (da) neurons. These neurons are classified into 4 types based on their dendrite branch complexity. I used the most simple ddaE classI and most complex ddaC classIV neurons in the experiments. DdaC neurons go through dendrite remodeling during the pupae stage. This characteristic of ddaC neurons allows me to compare three types of degeneration, including injury-induced axon degeneration, injury-induced dendrite degeneration and developmental pruning, in the same cell type on a single cell level of a living animal. Our lab developed a laser-cutting assay to precisely sever the dendrites or the axons proximal to the soma in whole, live Drosophila larvae. I observed that both axons and dendrites are able to initiate a rapid intrinsic program to clear the severely damaged part in a short period of time. Interestingly, I found that these processes looked similar to developmental pruning, in which dendrites of ddaC neurons are severed near soma and then quickly degraded within 18 hours after pupae formation. Due to this morphological similarity, I first wanted to know whether these processes share common machineries. I tested known pathways that have been reported to be involved in dendrite pruning. However, I discovered that none of these pathways had an effect on injury-induced degeneration. I concluded that axons and dendrites each have their own disassembly machinery that is activated by damage and is distinct from the ones employed in dendrite pruning. iv I next wanted to investigate the intracellular mediators involved in each injury-induced degeneration. I have observed fragmentation of microtubules during axon and dendrite degeneration. Additionally, our lab has done extensive work on microtubule polarity research. I decided to focus on the regulation of microtubules during degeneration. As an important component of neuron cytoskeleton, microtubules play a crucial role in cargo transport and cell shape maintenance. The role of microtubules in neuronal degeneration remains mysterious. I performed a genetic screen of all the potential microtubule severing proteins and microtubule depolymerizing proteins, and I identified two proteins, klp59C and fidgetin, involved in neuron degeneration. Klp59C, a microtubule-depolymerizing protein, serves as a general microtubule regulator involved in all types of degeneration. In contrast, fidgetin, a microtubule severing protein, is specifically required in dendrite degeneration. I further confirmed the RNAi result by repeating the same cutting assay in mutant and deficiency flies. Additionally, I investigated the working mechanism of klp59C and fidgetin through an EB1 comet assay. I found that EB1 dynamics lasted longer in klp59C knockdown neurons while EB1 dynamics disappeared around the same time in controls and fidgetin RNAi neurons. I thus concluded that fidgetin severs the microtubule in the middle to generate short fragments and klp59C further depolymerizes the microtubule fragments from the plus ends. Through a large-scale screen of potential pathways responsible for protein and organelle turnover during degeneration, I also discovered a new role of Rab GTPase. Rab5 or Rab11 GFP, which are usually used as an endocytosis marker, can serve as an energy monitor in live cells. I first observed that Rab5 GTP altered its punctate morphology to a diffused distribution 3.5h after axon severing. I also observed that all the other Rab GTPase family members, including Rab7, Rab8 and Rab11, share the same pattern after axon injury. Furthermore, I confirmed the observation that Rab protein changes v its morphology after ATP depletion in Hela cell cultures. This is the first time that the function of Rab as an energy indicator has been observed. In my work, I also examined whether the autophagy pathway and the endocytosis pathway are required for neuron degeneration. Down regulating the key proteins in both pathways through RNAi did not delay injury- induced axon or dendrite degeneration. However, I discovered that a decrease in the protein level of VPS4 and shrb (ESCRTIII in fly) significantly affects normal developmental pruning. This result provides additional evidence that developmental pruning and injury –induced degeneration are distinct processes, which involve different machineries. My work presented here demonstrated that microtubule regulators play important roles in degrading injured axons or dendrites. Klp59C plays a general role in all types of degeneration while fidgetin only acts in dendrite degeneration. Future work elucidating other pathways responsible for the degradation of other components of neurons will be crucial to dissect the comprehensive network of neuron disassembly after injury or in developmental settings. vi Table of Contents List of Figures ...................................................................................................................................x Acknowledgements.........................................................................................................................xiii Chapter 1. Introduction…………………………………………………………………………….1 Overview of neuron degeneration………………………………........................................1 Comparison of injury-induced degeneration and developmental pruning………………...7 Ubiquitin-proteasom System (UPS) in neuron degeneration...................................7 Wlds distinguishes the two processes......................................................................8 Other players separate the two processes.................................................................9 Microtubule degradation in a degeneration neuron.............................................................10 Energy maintenance and neuron degeneration....................................................................12 Summary…………………………………………………………………………………..15 References………………………………............................................................................17 Chapter 2. Dendrites have an active program of injury-induced degeneration that is molecularly distinct from developmental pruning....................................................................................21 Abstract.................................................................................................................................21 Introduction...........................................................................................................................21 Results..................................................................................................................................23 Dendrites undergo beading and clearance within 24 hours after severing...............23 Dendrite degeneration is blocked by overexpression of Wlds or UBP2..................27 Dendrite degeneration is independent of mitochondria............................................29 Dendrite degeneration is independent of apoptosis machinery.................................30 vii The pruning machinery is not required for injury-induced dendrite degeneration.................................................................................................35 Discussion............................................................................................................................37 Materials and Methods, Author Information, Acknowledgements......................................40 References............................................................................................................................42 Supplementary Materials......................................................................................................44 Chapter 3. Kinesin-13 terminates microtubule dynamics in degenerating axons before energy collapse...............................................................................................................................46 Abstract...............................................................................................................................46 Introduction.........................................................................................................................47
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