Search

Microtubules tightly regulate various cellular activities. Our understanding of microtubules is largely based on experiments using microtubule‐targeting agents, which, however, are insufficient to dissect the dynamic mechanisms of specific microtubule populations, due to their slow effects on the entire pool of microtubules. To overcome this technological limitation, we have used chemo and optogenetics to disassemble specific microtubule subtypes, including tyrosinated microtubules, primary cilia, mitotic spindles, and intercellular bridges, by rapidly recruiting engineered microtubule‐cleaving enzymes onto target microtubules in a reversible manner. Using this approach, we show that acute microtubule disassembly swiftly halts vesicular trafficking and lysosomal dynamics. It also immediately triggers Golgi and ER reorganization and slows the fusion/fission of mitochondria without affecting mitochondrial membrane potential. In addition, cell rigidity is increased after microtubule disruption owing to increased contractile stress fibers. Microtubule disruption furthermore prevents cell division, but does not cause cell death during interphase. Overall, the reported tools facilitate detailed analysis of how microtubules precisely regulate cellular architecture and functions. SYNOPSIS: Characterization of microtubules in cells via microtubule‐targeting agents is not ideal for assessing dynamics of specific microtubule populations. Here, a novel approach using an engineered microtubule‐severing enzyme allows spatiotemporal manipulation of microtubule disassembly triggered by either chemicals or illumination. A triple glutamine mutation in Spastin (dNSpastin3Q) reduces its association with microtubules.Engineered dNSpastin3Q acts as a microtubule‐severing enzyme in living cells.Recruitment of dNSpastin3Q to microtubules can be controlled by chemical‐ or light‐induced dimerization.Induced dimerization of dNSpastin3Q leads to acute disassembly of target microtubule subtypes. [ABSTRACT FROM AUTHOR]

The introduction of co‐dopants is one of the effective ways to improve the luminescence properties of the persistent luminescence nanoparticles (PLNPs). Herein, Cr3+, Ca2+ co‐doped and Cr3+, Ca2+, Pr3+ tri‐doped β‐Ga2O3 PLNPs with enhanced persistent luminescence were developed via the hydrothermal synthesis and subsequent calcinations, which improved the persistent luminescence of the β‐Ga2O3 PLNPs. The results showed that the prepared PLNPs had a long afterglow time of more than 8 days with a signal‐to‐noise ratio (SNR) of 272 and the Quantum yield (QY) up to 74.8 %, which was renewable by LED lamps and stored information under a high‐temperature environment. The synthesized β‐Ga2O3:Cr3+, Ca2+, Pr3+ PLNPs with long afterglow time showed great potentials in optical storage. [ABSTRACT FROM AUTHOR]

Macrophage depletion or LOX inhibition attenuated obesity-induced LOX and AT stiffening. (D) Immunoblot analysis of pro-LOX and LOX; and (E) LOX enzymatic activity in the cell lysates and culture medium of peritoneal macrophages derived from 10~12 week-old male mice (n = 3 in each group). The involvement of LOX and macrophage in adipose tissue stiffening and metabolism was dissected with LOX inhibition by BAPN and macrophage depletion by clodronate. Obesity is associated with adipose tissue (AT) fibrosis with aggregation or crosslinking of collagen fibers.1,2 Lysyl oxidase (LOX) gives rise to collagen crosslinking, while upregulated LOX is reported in AT of obese humans and mice.3,4 Our data showed higher second harmonic generation signals as well as collagen crosslinks in I ob/ob i AT than wild-type (WT) AT (Figure 1A and B). [Extracted from the article]

Mrf4 is a basic helix-loop-helix (bHLH) transcription factor associated with myogenesis. Two mrf4 transcripts, mrf4_tv1 and mrf4_tv2, were identified in zebrafish generated by alternative splicing. To study their biological functions, we separately injected the Mrf4-morpholinos, including MO1 ( mrf4_tv1:mrf4_tv2 knockdown), MO2+MO3 ( mrf4_tv1:mrf4_tv2 knockdown), MO3 ( mrf4_tv1 knockdown), and MO4 ( mrf4_tv2 knockdown), into zebrafish embryos to observe mrf4 gene knockdown phenotypes. No phenotypic abnormalities were observed following injection with 0.5 ng of MO1 but those injected with 4.5, 9, or 13.5 ng displayed curved-body phenotypes, such as indistinct somite boundaries, and a lack of uniformly sized cell blocks. Similar results were also observed in the (MO2+MO3)-, MO3-, and MO4-injected groups. To further investigate the molecular mechanisms that lead to curved-body phenotypes, we stained embryos with α-bungrotoxin and specific monoclonal antibodies F59, Znp1, and Zn5 to detect morphological changes in acetyl-choline receptor (AChR) clusters, muscle fibers, common path of the primary neurons, and secondary neurons axonal projections, respectively. Our results show that the muscle fibers of mrf4 _( tv1:tv2)-morphant aligned disorderly and lost their integrity and attachment, while the defects became milder in either mrf4_tv1-morphant or mrf4_tv2-morphant. On the other hand, reduced axonal projections and AChR clusters were found in both mrf4_tv2-morphant and mrf4 _( tv1:tv2)-morphant but distributed normally in the mrf4_tv1-morphant. We conclude that Mrf4_tv2 is involved in alignment of muscle fibers, and Mrf4_tv1 might have cooperative function with Mrf4_tv2 in muscle fiber alignment, without affecting the muscle-nerve connection. Developmental Dynamics 237:1043-1050, 2008. © 2008 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

The K+ ion in the title compound, [K(C14H10Cl2NO2)(H2O)4] n, is six-coordinated by five water mol­ecules and one [2-(2,6-dichloro­anilino)phen­yl]acetate ligand. Bridging by one of the four water mol­ecules in the asymmetric unit gives an infinite chain running along the b axis. [ABSTRACT FROM AUTHOR]