Publications

Google Scholar

https://scholar.google.com/citations?hl=en&user=_ZLy6tEAAAAJ&view_op=list_works&sortby=pubdate

Selected Publications

Jeng, JY, Carlton, AJ, Goodyear, RJ, Chinowsky, C, Ceriani, F, Johnson, SL, Sung, TS, Dayn, Y, Richardson, GP, Bowl, MR, Brown, SDM, Manor, U*, Marcotti, W AAV-mediated rescue of Eps8 expression in vivo restores hair-cell function in a mouse model of recessive deafness (2022) Molecular Therapy-Methods & Clinical Development.:355-370 *co-senior author DOI: https://doi.org/10.1016/j.omtm.2022.07.012

Fang L, Monroe F, Novak SW, Kirk L, Schiavon CR, Seungyoon BY, Zhang T, Wu M, Kastner K, Latif AA, Lin Z, Shaw A, Kubota Y, Mendenhall J, Zhang Z, Pekkurnaz G, Harris K, Howard J, Manor U. 2021. Deep learning-based point-scanning super-resolution imaging. Nat Methods, 18(4), 406-416.
(Featured in STATnews, PreLights, and KUSI). PMCID: PMC8035334

Schiavon C, Zhang T, Zhao B, Moore AS, Wales P, Andrade L, Wu M, Sung T-C, Dayn Y, Feng JW, Quintero OA, Shadel GS, Grosse R, Manor U. 2020. Actin chromobody imaging reveals sub-organellar actin dynamics. Nat Methods 17(9):917-921.
(Featured in PreLights) PMCID: PMC7746311.

Manor U, Bartholomew S, Golani G, Christenson E, Kozlov M, Higgs H, Spudich J, Lippincott-Schwartz J. 2015. A mitochondria-anchored isoform of the actin-nucleating spire protein regulates mitochondrial division. eLife 4. PMCID: PMC4574297.

Manor U, Disanza A, Grati M, Andrade L, Lin H, Di Fiore P, Scita G, Kachar B. 2011. Regulation of Stereocilia Length by Myosin XVa and Whirlin Depends on the Actin-Regulatory Protein Eps8. Curr Biol 21(2):167-172. PMCID: PMC3040242.

all Publications

Glavis-Bloom, C., Vanderlip, C., Weiser Novak, S., Kuwajima, M., Kirk, L., Harris, K.M., Manor, U., Reynolds, J.H. Violation of the ultrastructural size principle in the dorsolateral prefrontal cortex underlies working memory impairment in the aged common marmoset (Callithrix jacchus) (2023) Frontiers in Aging Neuroscience. 15. DOI: doi.org/10.3389/fnagi.2023.1146245

+ expand abstract

Morphology and function of the dorsolateral prefrontal cortex (dlPFC), and corresponding working memory performance, are affected early in the aging process, but nearly half of aged individuals are spared of working memory deficits. Translationally relevant model systems are critical for determining the neurobiological drivers of this variability. The common marmoset (Callithrix jacchus) is advantageous as a model for these investigations because, as a non-human primate, marmosets have a clearly defined dlPFC that enables measurement of prefrontal-dependent cognitive functions, and their short (∼10 year) lifespan facilitates longitudinal studies of aging. Previously, we characterized working memory capacity in a cohort of marmosets that collectively covered the lifespan, and found age-related working memory impairment. We also found a remarkable degree of heterogeneity in performance, similar to that found in humans. Here, we tested the hypothesis that changes to synaptic ultrastructure that affect synaptic efficacy stratify marmosets that age with cognitive impairment from those that age without cognitive impairment. We utilized electron microscopy to visualize synapses in the marmoset dlPFC and measured the sizes of boutons, presynaptic mitochondria, and synapses. We found that coordinated scaling of the sizes of synapses and mitochondria with their associated boutons is essential for intact working memory performance in aged marmosets. Further, lack of synaptic scaling, due to a remarkable failure of synaptic mitochondria to scale with presynaptic boutons, selectively underlies age-related working memory impairment. We posit that this decoupling results in mismatched energy supply and demand, leading to impaired synaptic transmission. We also found that aged marmosets have fewer synapses in dlPFC than young, though the severity of synapse loss did not predict whether aging occurred with or without cognitive impairment. This work identifies a novel mechanism of synapse dysfunction that stratifies marmosets that age with cognitive impairment from those that age without cognitive impairment. The process by which synaptic scaling is regulated is yet unknown and warrants future investigation.

Malik, N., Ferreira, B.I., Hollstein, P.E., Curtis, S.D., Trefts, E., Weiser Novak, S., Yu, J., Gilson, R., Hellberg, K., Fang, L., Sheridan, A., Hah, N., Shadel, G.S., Manor, U., Shaw, R.J. Induction of lysosomal and mitochondrial biogenesis by AMPK phosphorylation of FNIP1. (2023) Science. 380(6642):eabj5559. DOI: 10.1126/science.abj5559

+ expand abstract

Pham, T.B., Boussaty, E.C., Currais, A., Maher, P., Schubert, D.R., Manor, U., Friedman, R.A. Attenuation of Age-Related Hearing Impairment in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice Treated with Fatty Acid Synthase Inhibitor CMS121. (2023) Journal of Molecular Neuroscience. DOI: 10.1007/s12031-023-02119-w

+ expand abstract

Sheridan, A., Nguyen, T.M., Deb, D., Lee, W.A., Saalfeld, S., Turaga, S.C., Manor, U., Funke, J. Local shape descriptors for neuron segmentation. (2022) Nature Methods. DOI: 10.1038/s41592-022-01711-z

+ expand abstract

Shang, F., Wang, S.C., Gongol, B., Han, S.Y., Cho, Y., Schiavon, C.R., Chen, L., Xing, Y., Zhao, Y., Ning, M., Guo, X., He, F., Lei, Y., Wang, L., Manor, U., Marin, T., Chou, K.T., He, M., Huang, P.H., Shyy, J.Y., Malhotra, A. Obstructive Sleep Apnea-induced Endothelial Dysfunction is Mediated by miR-210. (2022) Am J Respir Crit Care Med. DOI: 10.1164/rccm.202202-0394OC

+ expand abstract

Calabrese, B., Jones, S.L., Shiraishi-Yamaguchi, Y., Lingelbach, M., Manor, U., Svitkina, T.M., Higgs, H.N., Shih, A.Y., Halpain, S. INF2-mediated actin filament reorganization confers intrinsic resilience to neuronal ischemic injury. (2022) Nature Communications. 13(1):6037. DOI: 10.1038/s41467-022-33268-y

+ expand abstract

Jeng, J.Y., Carlton, A.J., Goodyear, R.J., Chinowsky, C., Ceriani, F., Johnson, S.L., Sung, T.S., Dayn, Y., Richardson, G.P., Bowl, M.R., Brown, S.D.M., Manor, U., Marcotti, W. AAV-mediated rescue of Eps8 expression in vivo restores hair-cell function in a mouse model of recessive deafness (2022) Molecular Therapy-Methods & Clinical Development.:355-370 DOI: https://doi.org/10.1016/j.omtm.2022.07.012

+ expand abstract

Ramirez, M.A., Ninoyu, Y., Miller, C., Andrade, L.R., Edassery, S., Bomba-Warczak, E., Ortega, B., Manor, U., Rutherford, M.A., Friedman, R.A., Savas, J.N. Cochlear ribbon synapse maturation requires Nlgn1 and Nlgn3. (2022) iScience. 25(8):104803. DOI: 10.1016/j.isci.2022.104803

+ expand abstract

Chassefeyre, R., Chaiamarit, T., Verhelle, A., Novak, S.W., Andrade, L.R., Leitão, A.D.G., Manor, U., Encalada, S.E. Endosomal sorting drives the formation of axonal prion protein endoggresomes. (2021) Science Advances. 7(52):eabg3693. DOI: 10.1126/sciadv.abg3693

+ expand abstract

Ma, Z., Lytle, N.K., Chen, B., Jyotsana, N., Novak, S.W., Cho, C.J., Caplan, L., Ben-Levy, O., Neininger, A.C., Burnette, D.T., Trinh, V.Q., Tan, M.C.B., Patterson, E.A., Arrojo E Drigo, R., Giraddi, R.R., Ramos, C., Means, A.L., Matsumoto, I., Manor, U., Mills, J.C., Goldenring, J.R., Lau, K.S., Wahl, G.M., DelGiorno, K.E. Single-cell transcriptomics reveals a conserved metaplasia program in pancreatic injury. (2021) Gastroenterology. DOI: 10.1053/j.gastro.2021.10.027

+ expand abstract

Shadel, G.S., Adams, P.D., Berggren, W.T., Diedrich, J.K., Diffenderfer, K.E., Gage, F.H., Hah, N., Hansen, M., Hetzer, M.W., Molina, A.J.A., Manor, U., Marek, K., O’Keefe, D.D., Pinto, A.F.M., Sacco, A., Sharpee, T.O., Shokriev, M.N., Zambetti, S. The San Diego Nathan Shock Center: tackling the heterogeneity of aging. (2021) Geroscience. DOI: 10.1007/s11357-021-00426-x

+ expand abstract

Understanding basic mechanisms of aging holds great promise for developing interventions that prevent or delay many age-related declines and diseases simultaneously to increase human healthspan. However, a major confounding factor in aging research is the heterogeneity of the aging process itself. At the organismal level, it is clear that chronological age does not always predict biological age or susceptibility to frailty or pathology. While genetics and environment are major factors driving variable rates of aging, additional complexity arises because different organs, tissues, and cell types are intrinsically heterogeneous and exhibit different aging trajectories normally or in response to the stresses of the aging process (e.g., damage accumulation). Tackling the heterogeneity of aging requires new and specialized tools (e.g., single-cell analyses, mass spectrometry-based approaches, and advanced imaging) to identify novel signatures of aging across scales. Cutting-edge computational approaches are then needed to integrate these disparate datasets and elucidate network interactions between known aging hallmarks. There is also a need for improved, human cell-based models of aging to ensure that basic research findings are relevant to human aging and healthspan interventions. The San Diego Nathan Shock Center (SD-NSC) provides access to cutting-edge scientific resources to facilitate the study of the heterogeneity of aging in general and to promote the use of novel human cell models of aging. The center also has a robust Research Development Core that funds pilot projects on the heterogeneity of aging and organizes innovative training activities, including workshops and a personalized mentoring program, to help investigators new to the aging field succeed. Finally, the SD-NSC participates in outreach activities to educate the general community about the importance of aging research and promote the need for basic biology of aging research in particular.

Fang, L., Monroe, F., Novak, S.W., Kirk, L., Schiavon, C.R., Yu, S.B., Zhang, T., Wu, M., Kastner, K., Latif, A.A., Lin, Z., Shaw, A., Kubota, Y., Mendenhall, J., Zhang, Z., Pekkurnaz, G., Harris, K., Howard, J., Manor, U. Deep learning-based point-scanning super-resolution imaging. (2021) Nature Methods. DOI: 10.1038/s41592-021-01080-z

+ expand abstract

Lei, Y., Zhang, J., Schiavon, C.R., He, M., Chen, L., Shen, H., Zhang, Y., Yin, Q., Cho, Y., Andrade, L., Shadel, G.S., Hepokoski, M., Lei, T., Wang, H., Zhang, J., Yuan, J.X., Malhotra, A., Manor, U., Wang, S., Yuan, Z.Y., Shyy, J.Y. SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE2. (2021) Circulation research. DOI: 10.1161/CIRCRESAHA.121.318902

Schiavon, C.R., Shadel, G.S., Manor, U. Impaired Mitochondrial Mobility in Charcot-Marie-Tooth Disease. (2021) Front Cell Dev Biol. 9:624823. DOI: 10.3389/fcell.2021.624823

+ expand abstract

Lehman, B.J., Lopez-Diaz, F.J., Santisakultarm, T.P., Fang, L., Shokhirev, M.N., Diffenderfer, K.E., Manor, U., Emerson, B.M. Dynamic regulation of CTCF stability and sub-nuclear localization in response to stress. (2021) PLOS Genetics. 17(1):e1009277. DOI: 10.1371/journal.pgen.1009277

+ expand abstract

The nuclear protein CCCTC-binding factor (CTCF) has diverse roles in chromatin architecture and gene regulation. Functionally, CTCF associates with thousands of genomic sites and interacts with proteins, such as cohesin, or non-coding RNAs to facilitate specific transcriptional programming. In this study, we examined CTCF during the cellular stress response in human primary cells using immune-blotting, quantitative real time-PCR, chromatin immunoprecipitation-sequence (ChIP-seq) analysis, mass spectrometry, RNA immunoprecipitation-sequence analysis (RIP-seq), and Airyscan confocal microscopy. Unexpectedly, we found that CTCF is exquisitely sensitive to diverse forms of stress in normal patient-derived human mammary epithelial cells (HMECs). In HMECs, a subset of CTCF protein forms complexes that localize to Serine/arginine-rich splicing factor (SC-35)-containing nuclear speckles. Upon stress, this species of CTCF protein is rapidly downregulated by changes in protein stability, resulting in loss of CTCF from SC-35 nuclear speckles and changes in CTCF-RNA interactions. Our ChIP-seq analysis indicated that CTCF binding to genomic DNA is largely unchanged. Restoration of the stress-sensitive pool of CTCF protein abundance and re-localization to nuclear speckles can be achieved by inhibition of proteasome-mediated degradation. Surprisingly, we observed the same characteristics of the stress response during neuronal differentiation of human pluripotent stem cells (hPSCs). CTCF forms stress-sensitive complexes that localize to SC-35 nuclear speckles during a specific stage of neuronal commitment/development but not in differentiated neurons. We speculate that these particular CTCF complexes serve a role in RNA processing that may be intimately linked with specific genes in the vicinity of nuclear speckles, potentially to maintain cells in a certain differentiation state, that is dynamically regulated by environmental signals. The stress-regulated activity of CTCF is uncoupled in persistently stressed, epigenetically re-programmed “variant” HMECs and certain cancer cell lines. These results reveal new insights into CTCF function in cell differentiation and the stress-response with implications for oxidative damage-induced cancer initiation and neuro-degenerative diseases.

Schiavon, C.R., Zhang, T., Zhao, B., Moore, A.S., Wales, P., Andrade, L.R., Wu, M., Sung, T.C., Dayn, Y., Feng, J.W., Quintero, O.A., Shadel, G.S., Grosse, R., Manor, U. Actin chromobody imaging reveals sub-organellar actin dynamics. (2020) Nature Methods. DOI: 10.1038/s41592-020-0926-5

+ expand abstract

Pan, X., Fang, L., Liu, J., Senay-Aras, B., Lin, W., Zheng, S., Zhang, T., Guo, J., Manor, U., Van Norman, J., Chen, W., Yang, Z. Auxin-induced signaling protein nanoclustering contributes to cell polarity formation. (2020) Nature Communications. 11(1):3914. DOI: 10.1038/s41467-020-17602-w

+ expand abstract

Boussaty, E.C., Gillard, D., Lavinsky, J., Salehi, P., Wang, J., Mendonça, A., Allayee, H., Manor, U., Friedman, R.A. The Genetics of Variation of the Wave 1 Amplitude of the Mouse Auditory Brainstem Response. (2020) J Assoc Res Otolaryngol. 21(4):323-336. DOI: 10.1007/s10162-020-00762-3

+ expand abstract

This is the first genome-wide association study with the Hybrid Mouse Diversity Panel (HDMP) to define the genetic landscape of the variation in the suprathreshold wave 1 amplitude of the auditory brainstem response (ABR) both pre- and post-noise exposure. This measure is correlated with the density of the auditory neurons (AN) and/or the compliment of synaptic ribbons within the inner hair cells of the mouse cochlea. We analyzed suprathreshold ABR for 635 mice from 102 HMDP strains pre- and post-noise exposure (108 dB 10 kHz octave band noise exposure for 2 h) using auditory brainstem response (ABR) wave 1 suprathreshold amplitudes as part of a large survey (Myint et al., Hear Res 332:113-120, 2016). Genome-wide significance levels for pre- and post-exposure wave 1 amplitude across the HMDP were performed using FaST-LMM. Synaptic ribbon counts (Ctbp2 and mGluR2) were analyzed for the extreme strains within the HMDP. ABR wave 1 amplitude varied across all strains of the HMDP with differences ranging between 2.42 and 3.82-fold pre-exposure and between 2.43 and 7.5-fold post-exposure with several tone burst stimuli (4 kHz, 8 kHz, 12 kHz, 16 kHz, 24 kHz, and 32 kHz). Immunolabeling of paired synaptic ribbons and glutamate receptors of strains with the highest and lowest wave 1 values pre- and post-exposure revealed significant differences in functional synaptic ribbon counts. Genome-wide association analysis identified genome-wide significant threshold associations on chromosome 3 (24 kHz; JAX00105429; p < 1.12E-06) and chromosome 16 (16 kHz; JAX00424604; p < 9.02E-07) prior to noise exposure and significant associations on chromosomes 2 (32 kHz; JAX00497967; p < 3.68E-08) and 13 (8 kHz; JAX00049416; 1.07E-06) after noise exposure. In order to prioritize candidate genes, we generated cis-eQTLs from microarray profiling of RNA isolated from whole cochleae in 64 of the tested strains.This is the first report of a genome-wide association analysis, controlled for population structure, to explore the genetic landscape of suprathreshold wave 1 amplitude measurements of the mouse ABR. We have defined two genomic regions associated with wave 1 amplitude variation prior to noise exposure and an additional two associated with variation after noise exposure.

DelGiorno, K.E., Chung, C.Y., Vavinskaya, V., Maurer, H.C., Novak, S.W., Lytle, N.K., Ma, Z., Giraddi, R.R., Wang, D., Fang, L., Naeem, R.F., Andrade, L.R., Ali, W.H., Tseng, H., Tsui, C., Gubbala, V.B., Ridinger-Saison, M., Ohmoto, M., Erikson, G.A., O’Connor, C., Shokhirev, M.N., Hah, N., Urade, Y., Matsumoto, I., Kaech, S.M., Singh, P.K., Manor, U., Olive, K.P., Wahl, G.M. Tuft Cells Inhibit Pancreatic Tumorigenesis in Mice by Producing Prostaglandin D2. (2020) Gastroenterology. DOI: 10.1053/j.gastro.2020.07.037

+ expand abstract

Badgley, M.A., Kremer, D.M., Maurer, H.C., DelGiorno, K.E., Lee, H.J., Purohit, V., Sagalovskiy, I.R., Ma, A., Kapilian, J., Firl, C.E.M., Decker, A.R., Sastra, S.A., Palermo, C.F., Andrade, L.R., Sajjakulnukit, P., Zhang, L., Tolstyka, Z.P., Hirschhorn, T., Lamb, C., Liu, T., Gu, W., Seeley, E.S., Stone, E., Georgiou, G., Manor, U., Iuga, A., Wahl, G.M., Stockwell, B.R., Lyssiotis, C.A., Olive, K.P. Cysteine depletion induces pancreatic tumor ferroptosis in mice. (2020) Science. 368(6486):85-89. DOI: 10.1126/science.aaw9872

+ expand abstract

DelGiorno, K.E., Naeem, R.F., Fang, L., Chung, C.Y., Ramos, C., Luhtala, N., O’Connor, C., Hunter, T., Manor, U., Wahl, G.M. Tuft Cell Formation Reflects Epithelial Plasticity in Pancreatic Injury: Implications for Modeling Human Pancreatitis. (2020) Frontiers in Physiology. 11:88. DOI: 10.3389/fphys.2020.00088

+ expand abstract

Chu, Q., Martinez, T.F., Novak, S.W., Donaldson, C.J., Tan, D., Vaughan, J.M., Chang, T., Diedrich, J.K., Andrade, L., Kim, A., Zhang, T., Manor, U., Saghatelian, A. Regulation of the ER stress response by a mitochondrial microprotein. (2019) Nature Communications. 10(1):4883. DOI: 10.1038/s41467-019-12816-z

+ expand abstract

Villanueva, J.E., Livelo, C., Trujillo, A.S., Chandran, S., Woodworth, B., Andrade, L., Le, H.D., Manor, U., Panda, S., Melkani, G.C. Time-restricted feeding restores muscle function in Drosophila models of obesity and circadian-rhythm disruption. (2019) Nature Communications. 10(1):2700. DOI: 10.1038/s41467-019-10563-9

+ expand abstract

Shi, Y., Gao, W., Lytle, N.K., Huang, P., Yuan, X., Dann, A.M., Ridinger-Saison, M., DelGiorno, K.E., Antal, C.E., Liang, G., Atkins, A.R., Erikson, G., Sun, H., Meisenhelder, J., Terenziani, E., Woo, G., Fang, L., Santisakultarm, T.P., Manor, U., Xu, R., Becerra, C.R., Borazanci, E., Von Hoff, D.D., Grandgenett, P.M., Hollingsworth, M.A., Leblanc, M., Umetsu, S.E., Collisson, E.A., Scadeng, M., Lowy, A.M., Donahue, T.R., Reya, T., Downes, M., Evans, R.M., Wahl, G.M., Pawson, T., Tian, R., Hunter, T. Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring. (2019) Nature. 569(7754):131-135. DOI: 10.1038/s41586-019-1130-6

+ expand abstract

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis largely owing to inefficient diagnosis and tenacious drug resistance. Activation of pancreatic stellate cells (PSCs) and consequent development of dense stroma are prominent features accounting for this aggressive biology. The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains their own activation, facilitating a vicious cycle to exacerbate tumorigenesis and drug resistance. Furthermore, PSC activation occurs very early during PDAC tumorigenesis, and activated PSCs comprise a substantial fraction of the tumour mass, providing a rich source of readily detectable factors. Therefore, we hypothesized that the communication between PSCs and PCCs could be an exploitable target to develop effective strategies for PDAC therapy and diagnosis. Here, starting with a systematic proteomic investigation of secreted disease mediators and underlying molecular mechanisms, we reveal that leukaemia inhibitory factor (LIF) is a key paracrine factor from activated PSCs acting on cancer cells. Both pharmacologic LIF blockade and genetic Lifr deletion markedly slow tumour progression and augment the efficacy of chemotherapy to prolong survival of PDAC mouse models, mainly by modulating cancer cell differentiation and epithelial-mesenchymal transition status. Moreover, in both mouse models and human PDAC, aberrant production of LIF in the pancreas is restricted to pathological conditions and correlates with PDAC pathogenesis, and changes in the levels of circulating LIF correlate well with tumour response to therapy. Collectively, these findings reveal a function of LIF in PDAC tumorigenesis, and suggest its translational potential as an attractive therapeutic target and circulating marker. Our studies underscore how a better understanding of cell-cell communication within the tumour microenvironment can suggest novel strategies for cancer therapy.

Curchoe, C.L., Manor, U. Actin Cytoskeleton-Mediated Constriction of Membrane Organelles via Endoplasmic Reticulum Scaffolding. (2017) ACS Biomater Sci Eng. 3(11):2727-2732. DOI: 10.1021/acsbiomaterials.6b00802

+ expand abstract

Graydon, C.W., Manor, U., Kindt, K.S. In Vivo Ribbon Mobility and Turnover of Ribeye at Zebrafish Hair Cell Synapses. (2017) Scientific Reports. 7(1):7467. DOI: 10.1038/s41598-017-07940-z

+ expand abstract

Yao, P.J., Manor, U., Petralia, R.S., Brose, R.D., Wu, R.T., Ott, C., Wang, Y.X., Charnoff, A., Lippincott-Schwartz, J., Mattson, M.P. Sonic hedgehog pathway activation increases mitochondrial abundance and activity in hippocampal neurons. (2017) Molecular Biology of the Cell. 28(3):387-395. DOI: 10.1091/mbc.E16-07-0553

+ expand abstract

Andrade, L.R., Salles, F.T., Grati, M., Manor, U., Kachar, B. Tectorins crosslink type II collagen fibrils and connect the tectorial membrane to the spiral limbus. (2016) Journal of Structural Biology. 194(2):139-146. DOI: 10.1016/j.jsb.2016.01.006

+ expand abstract

Webster, M.T., Manor, U., Lippincott-Schwartz, J., Fan, C.M. Intravital Imaging Reveals Ghost Fibers as Architectural Units Guiding Myogenic Progenitors during Regeneration. (2016) Cell Stem Cell. 18(2):243-252. DOI: 10.1016/j.stem.2015.11.005

+ expand abstract

Manor, U., Bartholomew, S., Golani, G., Christenson, E., Kozlov, M., Higgs, H., Spudich, J., Lippincott-Schwartz, J. A mitochondria-anchored isoform of the actin-nucleating spire protein regulates mitochondrial division. (2015) Elife. 4. DOI: 10.7554/eLife.08828

+ expand abstract

Orly, G., Manor, U., Gov, N.S. A Biophysical Model for the Staircase Geometry of Stereocilia. (2015) PLOS One. 10(7):e0127926. DOI: 10.1371/journal.pone.0127926

+ expand abstract

Quintero, O.A., Unrath, W.C., Stevens, S.M., Manor, U., Kachar, B., Yengo, C.M. Myosin 3A kinase activity is regulated by phosphorylation of the kinase domain activation loop. (2013) Journal of Biological Chemistry. 288(52):37126-37137. DOI: 10.1074/jbc.M113.511014

+ expand abstract

Furness, D.N., Johnson, S.L., Manor, U., Rüttiger, L., Tocchetti, A., Offenhauser, N., Olt, J., Goodyear, R.J., Vijayakumar, S., Dai, Y., Hackney, C.M., Franz, C., Di Fiore, P.P., Masetto, S., Jones, S.M., Knipper, M., Holley, M.C., Richardson, G.P., Kachar, B., Marcotti, W. Progressive hearing loss and gradual deterioration of sensory hair bundles in the ears of mice lacking the actin-binding protein Eps8L2. (2013) Proceedings of the National Academy of Sciences of the United States of America. 110(34):13898-13903. DOI: 10.1073/pnas.1304644110

+ expand abstract

Ben Isaac, E., Manor, U., Kachar, B., Yochelis, A., Gov, N.S. Linking actin networks and cell membrane via a reaction-diffusion-elastic description of nonlinear filopodia initiation. (2013) Phys Rev E Stat Nonlin Soft Matter Phys. 88(2):022718. DOI: 10.1103/PhysRevE.88.022718

+ expand abstract

Manor, U., Grati, M., Yengo, C.M., Kachar, B., Gov, N.S. Competition and compensation: dissecting the biophysical and functional differences between the class 3 myosin paralogs, myosins 3a and 3b. (2012) Bioarchitecture. 2(5):171-174. DOI: 10.4161/bioa.21733

+ expand abstract

Merritt, R.C., Manor, U., Salles, F.T., Grati, M., Dose, A.C., Unrath, W.C., Quintero, O.A., Yengo, C.M., Kachar, B. Myosin IIIB uses an actin-binding motif in its espin-1 cargo to reach the tips of actin protrusions. (2012) Current Biology. 22(4):320-325. DOI: 10.1016/j.cub.2011.12.053

+ expand abstract

Manor, U., Disanza, A., Grati, M., Andrade, L., Lin, H., Di Fiore, P.P., Scita, G., Kachar, B. Regulation of stereocilia length by myosin XVa and whirlin depends on the actin-regulatory protein Eps8. (2011) Current Biology. 21(2):167-172. DOI: 10.1016/j.cub.2010.12.046

+ expand abstract

Quintero, O.A., Moore, J.E., Unrath, W.C., Manor, U., Salles, F.T., Grati, M., Kachar, B., Yengo, C.M. Intermolecular autophosphorylation regulates myosin IIIa activity and localization in parallel actin bundles. (2010) Journal of Biological Chemistry. 285(46):35770-35782. DOI: 10.1074/jbc.M110.144360

+ expand abstract

Salles, F.T., Merritt, R.C., Manor, U., Dougherty, G.W., Sousa, A.D., Moore, J.E., Yengo, C.M., Dosé, A.C., Kachar, B. Myosin IIIa boosts elongation of stereocilia by transporting espin 1 to the plus ends of actin filaments. (2009) Nature Cell Biology. 11(4):443-450. DOI: 10.1038/ncb1851

+ expand abstract

Naoz, M., Manor, U., Sakaguchi, H., Kachar, B., Gov, N.S. Protein localization by actin treadmilling and molecular motors regulates stereocilia shape and treadmilling rate. (2008) Biophysical Journal. 95(12):5706-5718. DOI: 10.1529/biophysj.108.143453

+ expand abstract

Manor, U., Kachar, B. Dynamic length regulation of sensory stereocilia. (2008) Seminars in Cell & Developmental Biology. 19(6):502-510. DOI: 10.1016/j.semcdb.2008.07.006

+ expand abstract

Taiber, S., Gozlan, O., Cohen, R., Andrade, L.R., Gregory, E.F., Starr, D.A., Moran, Y., Hipp, R., Kelley, M.W., Manor, U., Sprinzak, D., Avraham, K.B. A Nesprin-4/kinesin-1 cargo model for nuclear positioning in cochlear outer hair cells. (2022) Front Cell Dev Biol. 10:974168. DOI: 10.3389/fcell.2022.974168

+ expand abstract

Glavis-Bloom, C., Vanderlip, C.R., Weiser Novak, S., Kuwajima, M., Kirk, L., Harris, K.M., Manor, U., Reynolds, J.H. Violation of the ultrastructural size principle in the dorsolateral prefrontal cortex underlies working memory impairment in the aged common marmoset (Callithrix jacchus). (n.d.) Frontiers in Aging Neuroscience. 15:1146245. DOI: 10.3389/fnagi.2023.1146245

+ expand abstract