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Full-Text Articles in Life Sciences

Together, The Ift81 And Ift74 N-Termini Form The Main Module For Intraflagellar Transport Of Tubulin, Tomohiro Kubo, Jason Brown, Karl D. Bellve, Branch Craige, Julie M. Craft, Kevin E. Fogarty, Karl-Ferdinand Lechtreck, George B. Witman May 2016

Together, The Ift81 And Ift74 N-Termini Form The Main Module For Intraflagellar Transport Of Tubulin, Tomohiro Kubo, Jason Brown, Karl D. Bellve, Branch Craige, Julie M. Craft, Kevin E. Fogarty, Karl-Ferdinand Lechtreck, George B. Witman

Cell and Developmental Biology Publications

The assembly and maintenance of most cilia and flagella rely on intraflagellar transport (IFT). Recent in vitro studies have suggested that, together, the calponin-homology domain within the IFT81 N-terminus and the highly basic N-terminus of IFT74 form a module for IFT of tubulin. By using Chlamydomonas mutants for IFT81 and IFT74, we tested this hypothesis in vivo Modification of the predicted tubulin-binding residues in IFT81 did not significantly affect basic anterograde IFT and length of steady-state flagella but slowed down flagellar regeneration, a phenotype similar to that seen in a strain that lacks the IFT74 N-terminus. In both mutants, the ...


Global Gene Expression Profiling Of Jmjd6- And Jmjd4-Depleted Mouse Nih3t3 Fibroblasts, Yu-Jie Hu, Anthony N. Imbalzano Apr 2016

Global Gene Expression Profiling Of Jmjd6- And Jmjd4-Depleted Mouse Nih3t3 Fibroblasts, Yu-Jie Hu, Anthony N. Imbalzano

Cell and Developmental Biology Publications

Emerging evidence suggests Jumonji domain-containing proteins are epigenetic regulators in diverse biological processes including cellular differentiation and proliferation. RNA interference-based analyses combined with gene expression profiling can effectively characterize the cellular functions of these enzymes. We found that the depletion of Jumonji domain-containing protein 6 (JMJD6) and its paralog protein Jumonji domain-containing protein 4 (JMJD4) individually by small hairpin RNAs (shRNAs) slowed cell proliferation of mouse NIH3T3 fibroblasts. We subsequently performed gene expression profiling on both JMJD6- and JMJD4-depleted mouse NIH3T3 fibroblasts using the Affymetrix GeneChip Mouse Exon 1.0 ST Array. Here we report the gene profiling datasets along ...


Cfap54 Is Required For Proper Ciliary Motility And Assembly Of The Central Pair Apparatus In Mice, Casey W. Mckenzie, Branch Craige, Tiffany V. Kroeger, Rozzy Finn, Todd A. Wyatt, Joseph H. Sisson, Jacqueline A. Pavlik, Lara Strittmatter, Gregory M. Hendricks, George B. Witman, Lance Lee Sep 2015

Cfap54 Is Required For Proper Ciliary Motility And Assembly Of The Central Pair Apparatus In Mice, Casey W. Mckenzie, Branch Craige, Tiffany V. Kroeger, Rozzy Finn, Todd A. Wyatt, Joseph H. Sisson, Jacqueline A. Pavlik, Lara Strittmatter, Gregory M. Hendricks, George B. Witman, Lance Lee

Cell and Developmental Biology Publications

Motile cilia and flagella play critical roles in fluid clearance and cell motility, and dysfunction commonly results in the pediatric syndrome primary ciliary dyskinesia (PCD). CFAP221, also known as PCDP1, is required for ciliary and flagellar function in mice and Chlamydomonas reinhardtii, where it localizes to the C1d projection of the central microtubule apparatus and functions in a complex that regulates flagellar motility in a calcium-dependent manner. We demonstrate that the genes encoding the mouse homologues of the other C. reinhardtii C1d complex members are primarily expressed in motile ciliated tissues, suggesting a conserved function in mammalian motile cilia. The ...


Drc3 Connects The N-Drc To Dynein G To Regulate Flagellar Waveform, Junya Awata, Kangkang Song, Jianfeng Lin, Stephen M. King, Michael J. Sanderson, Daniela Nicastro, George B. Witman Aug 2015

Drc3 Connects The N-Drc To Dynein G To Regulate Flagellar Waveform, Junya Awata, Kangkang Song, Jianfeng Lin, Stephen M. King, Michael J. Sanderson, Daniela Nicastro, George B. Witman

Cell and Developmental Biology Publications

The nexin-dynein regulatory complex (N-DRC), which is a major hub for the control of flagellar motility, contains at least 11 different subunits. A major challenge is to determine the location and function of each of these subunits within the N-DRC. We characterized a Chlamydomonas mutant defective in the N-DRC subunit DRC3. Of the known N-DRC subunits, the drc3 mutant is missing only DRC3. Like other N-DRC mutants, the drc3 mutant has a defect in flagellar motility. However, in contrast to other mutations affecting the N-DRC, drc3 does not suppress flagellar paralysis caused by loss of radial spokes. Cryo-electron tomography revealed ...


Reduced Tubulin Polyglutamylation Suppresses Flagellar Shortness In Chlamydomonas, Tomohiro Kubo, Masafumi Hirono, Takumi Aikawa, Ritsu Kamiya, George B. Witman Aug 2015

Reduced Tubulin Polyglutamylation Suppresses Flagellar Shortness In Chlamydomonas, Tomohiro Kubo, Masafumi Hirono, Takumi Aikawa, Ritsu Kamiya, George B. Witman

Cell and Developmental Biology Publications

Ciliary length control is an incompletely understood process essential for normal ciliary function. The flagella of Chlamydomonas mutants lacking multiple axonemal dyneins are shorter than normal; previously it was shown that this shortness can be suppressed by the mutation suppressor of shortness 1 (ssh1) via an unknown mechanism. To elucidate this mechanism, we carried out genetic analysis of ssh1 and found that it is a new allele of TPG2 (hereafter tpg2-3), which encodes FAP234 functioning in tubulin polyglutamylation in the axoneme. Similar to the polyglutamylation-deficient mutants tpg1 and tpg2-1, tpg2-3 axonemal tubulin has a greatly reduced level of long polyglutamate ...


P53 Protects Against Genome Instability Following Centriole Duplication Failure, Bramwell G. Lambrus, Yumi Uetake, Kevin M. Clutario, Vikas Daggubati, Michael Snyder, Greenfield Sluder, Andrew J. Holland Jul 2015

P53 Protects Against Genome Instability Following Centriole Duplication Failure, Bramwell G. Lambrus, Yumi Uetake, Kevin M. Clutario, Vikas Daggubati, Michael Snyder, Greenfield Sluder, Andrew J. Holland

Cell and Developmental Biology Publications

Centriole function has been difficult to study because of a lack of specific tools that allow persistent and reversible centriole depletion. Here we combined gene targeting with an auxin-inducible degradation system to achieve rapid, titratable, and reversible control of Polo-like kinase 4 (Plk4), a master regulator of centriole biogenesis. Depletion of Plk4 led to a failure of centriole duplication that produced an irreversible cell cycle arrest within a few divisions. This arrest was not a result of a prolonged mitosis, chromosome segregation errors, or cytokinesis failure. Depleting p53 allowed cells that fail centriole duplication to proliferate indefinitely. Washout of auxin ...


Myosin-Binding Protein C Corrects An Intrinsic Inhomogeneity In Cardiac Excitation-Contraction Coupling, Michael J. Previs, Benjamin L. Prosser, Ji Young Mun, Samantha Beck Previs, James Gulick, Kyounghwan Lee, Jeffrey Robbins, Roger Craig, W J. Lederer, David M. Warshaw Feb 2015

Myosin-Binding Protein C Corrects An Intrinsic Inhomogeneity In Cardiac Excitation-Contraction Coupling, Michael J. Previs, Benjamin L. Prosser, Ji Young Mun, Samantha Beck Previs, James Gulick, Kyounghwan Lee, Jeffrey Robbins, Roger Craig, W J. Lederer, David M. Warshaw

Cell and Developmental Biology Publications

The beating heart exhibits remarkable contractile fidelity over a lifetime, which reflects the tight coupling of electrical, chemical, and mechanical elements within the sarcomere, the elementary contractile unit. On a beat-to-beat basis, calcium is released from the ends of the sarcomere and must diffuse toward the sarcomere center to fully activate the myosin- and actin-based contractile proteins. The resultant spatial and temporal gradient in free calcium across the sarcomere should lead to nonuniform and inefficient activation of contraction. We show that myosin-binding protein C (MyBP-C), through its positioning on the myosin thick filaments, corrects this nonuniformity in calcium activation by ...


Hdac4 Integrates Pth And Sympathetic Signaling In Osteoblasts, Arnaud Obri, Munevver Parla. Makinistoglu, Hong Zhang, Gerard Karsenty Jun 2014

Hdac4 Integrates Pth And Sympathetic Signaling In Osteoblasts, Arnaud Obri, Munevver Parla. Makinistoglu, Hong Zhang, Gerard Karsenty

Cell and Developmental Biology Publications

Parathyroid hormone (PTH) and the sympathetic tone promote Rankl expression in osteoblasts and osteoclast differentiation by enhancing cyclic adenosine monophosphate production through an unidentified transcription factor for PTH and through ATF4 for the sympathetic tone. How two extracellular cues using the same second messenger in the same cell elicit different transcriptional events is unknown. In this paper, we show that PTH favors Rankl expression by triggering the ubiquitination of HDAC4, a class II histone deacetylase, via Smurf2. HDAC4 degradation releases MEF2c, which transactivates the Rankl promoter. Conversely, sympathetic signaling in osteoblasts favors the accumulation of HDAC4 in the nucleus and ...