@article {56204, title = {A genetically encoded near-infrared fluorescent calcium ion indicator.}, journal = {Nature Methods}, volume = {16}, year = {2019}, month = {2019 Jan 21}, pages = {171-4}, abstract = {

We report an intensiometric, near-infrared fluorescent, genetically encoded calcium ion (Ca) indicator (GECI) with excitation and emission maxima at 678 and 704 nm, respectively. This GECI, designated NIR-GECO1, enables imaging of Ca transients in cultured mammalian cells and brain tissue with sensitivity comparable to that of currently available visible-wavelength GECIs. We demonstrate that NIR-GECO1 opens up new vistas for multicolor Ca imaging in combination with other optogenetic indicators and actuators.

}, issn = {1548-7105}, doi = {10.1038/s41592-018-0294-6}, author = {Qian, Yong and Piatkevich, Kiryl D and Mc Larney, Benedict and Abdelfattah, Ahmed S and Mehta, Sohum and Murdock, Mitchell H and Gottschalk, Sven and Molina, Rosana S and Zhang, Wei and Chen, Yingche and Wu, Jiahui and Drobizhev, Mikhail and Hughes, Thomas E and Zhang, Jin and Schreiter, Eric R and Shoham, Shy and Razansky, Daniel and Boyden, Edward S and Campbell, Robert E} } @article {48799, title = {Optogenetic control with a photocleavable protein, PhoCl.}, journal = {Nature Methods}, volume = {14}, year = {2017}, month = {2017 Apr}, pages = {391-394}, abstract = {

To expand the range of experiments that are accessible with optogenetics, we developed a photocleavable protein (PhoCl) that spontaneously dissociates into two fragments after violet-light-induced cleavage of a specific bond in the protein backbone. We demonstrated that PhoCl can be used to engineer light-activatable Cre recombinase, Gal4 transcription factor, and a viral protease that in turn was used to activate opening of the large-pore ion channel Pannexin-1.

}, keywords = {Connexins, Directed Molecular Evolution, Green Fluorescent Proteins, HEK293 Cells, HSP90 Heat-Shock Proteins, Humans, Luminescent Proteins, Nerve Tissue Proteins, Nuclear Localization Signals, Optogenetics, Patch-Clamp Techniques, Photochemistry, Protein Engineering, Recombinant Proteins, Viral Nonstructural Proteins}, issn = {1548-7105}, doi = {10.1038/nmeth.4222}, author = {Zhang, Wei and Lohman, Alexander W and Zhuravlova, Yevgeniya and Lu, Xiaocen and Wiens, Matthew D and Hoi, Hiofan and Yaganoglu, Sine and Mohr, Manuel A and Kitova, Elena N and Klassen, John S and Pantazis, Periklis and Thompson, Roger J and Campbell, Robert E} } @article {68443, title = {A Defensive Kicking Behavior in Response to Mechanical Stimuli Mediated by Drosophila Wing Margin Bristles.}, journal = {J Neurosci}, volume = {36}, year = {2016}, month = {11/2016}, pages = {11275-11282}, abstract = {

Mechanosensation, one of the fastest sensory modalities, mediates diverse behaviors including those pertinent for survival. It is important to understand how mechanical stimuli trigger defensive behaviors. Here, we report that Drosophila melanogaster adult flies exhibit a kicking response against invading parasitic mites over their wing margin with ultrafast speed and high spatial precision. Mechanical stimuli that mimic the mites{\textquoteright} movement evoke a similar kicking behavior. Further, we identified a TRPV channel, Nanchung, and a specific Nanchung-expressing neuron under each recurved bristle that forms an array along the wing margin as being essential sensory components for this behavior. Our electrophysiological recordings demonstrated that the mechanosensitivity of recurved bristles requires Nanchung and Nanchung-expressing neurons. Together, our results reveal a novel neural mechanism for innate defensive behavior through mechanosensation.

SIGNIFICANCE STATEMENT: We discovered a previously unknown function for recurved bristles on the Drosophila melanogaster wing. We found that when a mite (a parasitic pest for Drosophila) touches the wing margin, the fly initiates a swift and accurate kick to remove the mite. The fly head is dispensable for this behavior. Furthermore, we found that a TRPV channel, Nanchung, and a specific Nanchung-expressing neuron under each recurved bristle are essential for its mechanosensitivity and the kicking behavior. In addition, touching different regions of the wing margin elicits kicking directed precisely at the stimulated region. Our experiments suggest that recurved bristles allow the fly to sense the presence of objects by touch to initiate a defensive behavior (perhaps analogous to touch-evoked scratching; Akiyama et al., 2012).

}, keywords = {Animals, Avoidance Learning, Defense Mechanisms, Drosophila, Drosophila Proteins, Extremities, Mechanoreceptors, Mechanotransduction, Cellular, Physical Stimulation, Reflex, Sense Organs, Sensory Receptor Cells, Touch, Transient Receptor Potential Channels, Wings, Animal}, issn = {1529-2401}, doi = {10.1523/JNEUROSCI.1416-16.2016}, author = {Li, Jiefu and Zhang, Wei and Guo, Zhenhao and Wu, Sophia and Jan, Lily Yeh and Jan, Yuh-Nung} } @article {68445, title = {Transmembrane channel-like (tmc) gene regulates Drosophila larval locomotion.}, journal = {Proc Natl Acad Sci U S A}, volume = {113}, year = {2016}, month = {06/2016}, pages = {7243-8}, abstract = {

Drosophila larval locomotion, which entails rhythmic body contractions, is controlled by sensory feedback from proprioceptors. The molecular mechanisms mediating this feedback are little understood. By using genetic knock-in and immunostaining, we found that the Drosophila melanogaster transmembrane channel-like (tmc) gene is expressed in the larval class I and class II dendritic arborization (da) neurons and bipolar dendrite (bd) neurons, both of which are known to provide sensory feedback for larval locomotion. Larvae with knockdown or loss of tmc function displayed reduced crawling speeds, increased head cast frequencies, and enhanced backward locomotion. Expressing Drosophila TMC or mammalian TMC1 and/or TMC2 in the tmc-positive neurons rescued these mutant phenotypes. Bending of the larval body activated the tmc-positive neurons, and in tmc mutants this bending response was impaired. This implicates TMC{\textquoteright}s roles in Drosophila proprioception and the sensory control of larval locomotion. It also provides evidence for a functional conservation between Drosophila and mammalian TMCs.

}, keywords = {Animals, Animals, Genetically Modified, Cell Line, Drosophila melanogaster, Drosophila Proteins, Larva, Locomotion, Membrane Proteins, Mutation, Neurons}, issn = {1091-6490}, doi = {10.1073/pnas.1606537113}, author = {Guo, Yanmeng and Wang, Yuping and Zhang, Wei and Meltzer, Shan and Zanini, Damiano and Yu, Yue and Li, Jiefu and Cheng, Tong and Guo, Zhenhao and Wang, Qingxiu and Jacobs, Julie S and Sharma, Yashoda and Eberl, Daniel F and G{\"o}pfert, Martin C and Jan, Lily Yeh and Jan, Yuh Nung and Wang, Zuoren} } @article {68446, title = {Ankyrin Repeats Convey Force to Gate the NOMPC Mechanotransduction Channel.}, journal = {Cell}, volume = {162}, year = {2015}, month = {09/2015}, pages = {1391-403}, abstract = {

How metazoan mechanotransduction channels sense mechanical stimuli is not well understood. The NOMPC channel in the transient receptor potential (TRP) family, a mechanotransduction channel for Drosophila touch sensation and hearing, contains 29 Ankyrin repeats (ARs) that associate with microtubules. These ARs have been postulated to act as a tether that conveys force to the channel. Here, we report that these N-terminal ARs form a cytoplasmic domain essential for NOMPC mechanogating in vitro, mechanosensitivity of touch receptor neurons in vivo, and touch-induced behaviors of Drosophila larvae. Duplicating the ARs elongates the filaments that tether NOMPC to microtubules in mechanosensory neurons. Moreover, microtubule association is required for NOMPC mechanogating. Importantly, transferring the NOMPC ARs to mechanoinsensitive voltage-gated potassium channels confers mechanosensitivity to the chimeric channels. These experiments strongly support a tether mechanism of mechanogating for the NOMPC channel, providing insights into the basis of mechanosensitivity of mechanotransduction channels.

}, keywords = {Animals, Drosophila, Drosophila Proteins, Kv1.2 Potassium Channel, Larva, Mechanotransduction, Cellular, Microtubules, Protein Structure, Tertiary, Touch, Transient Receptor Potential Channels}, issn = {1097-4172}, doi = {10.1016/j.cell.2015.08.024}, author = {Zhang, Wei and Cheng, Li E and Kittelmann, Maike and Li, Jiefu and Petkovic, Maja and Cheng, Tong and Jin, Peng and Guo, Zhenhao and G{\"o}pfert, Martin C and Jan, Lily Yeh and Jan, Yuh Nung} }