Microfabricated elastomer tactile sensors for robotic fingertip systems

Tactile sensing is an important aspect of robotic systems, and enables safe, dexterous robot-environment interaction. The design and implementation of tactile sensors on robots has been a topic of research over the past 30 years, and current challenges include mechanically flexible “sensing skins”, high dynamic range (DR) sensing (i.e.: high force range and fine force resolution), multi-axis sensing, and integration between the sensors and robot. This dissertation focuses on addressing some of these challenges through a novel manufacturing process that incorporates conductive and dielectric elastomers in a reusable, multilength-scale mold, and new sensor designs for multi-axis sensing that improve force range without sacrificing resolution. A single taxel was integrated into a 1 degree of freedom robotic gripper for closed-loop slip detection. Manufacturing involved casting a composite silicone rubber, polydimethylsiloxane (PDMS) filled with conductive particles such as carbon nanotubes, into a mold to produce microscale flexible features on the order of 10s of microns. Molds were produced via microfabrication of silicon wafers, but were limited in sensing area and were costly. An improved technique was developed that produced molds of acrylic using a computer numerical controlled (CNC) milling machine. This maintained the ability to produce microscale features, and increased the sensing area while reducing costs. New sensing skins had features as small as 20 microns over an area as large as a human hand. Sensor architectures capable of sensing both shear and normal force sensing with high dynamic range were produced. Using this architecture, two sensing modalities were developed: a capacitive approach and a contact resistive approach. The capacitive approach demonstrated better dynamic range, while the contact resistive approach used simpler circuitry. Using the contact resistive approach, normal force range and resolution were 8,000 mN and 1,000 mN, respectively, and shear force range and resolution were 450 mN and 100 mN, respectively. Using the capacitive approach, normal force range and resolution were 10,000 mN and 100 mN, respectively, and shear force range and resolution were 1,500 mN and 50 mN, respectively.

CHARACTERIZATION OF TOBACCO MOSAIC VIRUS DIRECTED REPROGRAMMING OF PHLOEM GENE EXPRESSION TO PROMOTE VIRAL PHLOEM LOADING AND SYSTMEIC MOVEMENT

Vascular phloem loading has long been recognized as an essential step in the establishment of a systemic virus infection. Yet little is known about this process and the mechanisms that control it. In this study, an interaction between the replication protein of Tobacco mosaic virus (TMV) and phloem specific auxin/indole acetic acid (Aux/IAA) transcriptional regulators was found to modulate virus phloem loading. Promoter expression studies show TMV 126/183 kDa interacting Aux/IAAs predominantly express and accumulate within the nuclei of phloem companion cells (CC). Furthermore, CC Aux/IAA nuclear localization is disrupted upon infection with an interacting virus but not during infection with a non-interacting virus. In situ analysis of virus spread shows the inability of TMV variants to disrupt Aux/IAA CC nuclear localization correlates with a reduced ability to load into the vascular tissue. Subsequent systemic movement assays also demonstrate that a virus capable of disrupting Aux/IAA localization is significantly more competitive at systemic movement than a non-interacting virus. Similarly, CC expression and over-accumulation of a degradation-resistant-interacting Aux/IAA protein was found to selectively inhibit TMV accumulation and phloem loading. Transcriptional expression studies demonstrate a role for interacting Aux/IAA proteins in the regulation of salicylic acid and jasmonic acid dependent host defense responses as well as virus specific movement factors including pectin methylesterase that are involved in regulating plasmodesmata size exclusion limits and promoting virus cell-to-cell movement. Further characterization of the phloem environment was done using two phloem specific promoters (pSUC2 and pSULTR2;2) to generate epitope-tagged polysomal-RNA complexes. Immuno-purification using the epitope tag allowed us to obtain mRNAs bound to polysomes (the translatome) specifically in phloem tissue. We found the phloem translatome is uniquely altered during TMV infection with 90% and 88% of genes down regulated in the pSUC2 and pSULTR2;2 phloem translatomes, compared to 31% of genes down regulated in the whole plant p35S translatome. Transcripts down regulated in phloem include genes involved in callose deposition at plasmodesmata, host defense responses, and RNA silencing. Combined, these findings indicate TMV reprograms gene expression within the vascular phloem as a means to enhance phloem loading and systemic spread.