The R2R3 MYB genes associated with the flavonoid/anthocyanidin pathway feature two repeats, and represent the most abundant classes of MYB genes in plants; however, the physiological role and ...regulatory function of most R2R3 MYBs remain poorly understood in kiwifruit (
). Here, genome-wide analysis identified 155 R2R3-MYBs in the 'Red 5' version of the
genome. Out of 36 anthocyanin-related AccR2R3-MYBs,
was the most highly expressed in inner pericarp of red-fleshed kiwifruit. The expression of
was highly correlated with anthocyanin accumulation in natural pigmentation during fruit ripening and light-/temperature-induced pigmentation in the callus.
is localized in the nuclei and has transcriptional activation activity. Overexpression of
elevates anthocyanin accumulation in transgenic
. In comparison,
fruit infiltrated with virus-induced gene silencing showed delayed red coloration, lower anthocyanin content, and lower expression of
. The transient expression experiment in
leaves and
fruit indicated the interaction of
with
might strongly activate anthocyanin biosynthesis by activating the transcription of
and
. In conclusion, this study provides novel molecular information about R2R3-MYBs in kiwifruit, advances our understanding of light- and temperature-induced anthocyanin accumulation, and demonstrates the important function of
in the biosynthesis of anthocyanin in kiwifruit.
Improper kinetochore attachments activate the spindle assembly checkpoint (SAC) to prevent anaphase onset, but it is poorly understood how this checkpoint is silenced to allow anaphase onset. ...Chromosome bipolar attachment applies tension on sister kinetochores, and the lack of tension delays anaphase onset. In budding yeast, the delay induced by tension defects depends on the intact SAC as well as increase in ploidy (Ipl1)/Aurora kinase and a centromere-associated protein ShuGOshin (Sgo1). Here we provide evidence indicating that Ipl1-dependent phosphorylation of the kinetochore protein Duo1 and Mps1 interacting (Dam1) prevents SAC silencing when tension is absent. The nonphosphorylatable dam1 mutant cells, as well as sgo1 mutant cells, are competent in SAC activation but unable to prevent SAC silencing in response to tension defects. We further found that phosphomimetic dam1 mutants exhibited delayed anaphase onset mainly due to the failure in SAC silencing, but destabilized kinetochore attachment likely plays a minor role in this delay. Because the tension resulting from bipolar attachment triggers the dephosphorylation of Dam1 by protein phosphatase 1, this dephosphorylation likely coordinates SAC silencing with chromosome bipolar attachment. Therefore, Sgo1, Ipl1 kinase, Dam1, and protein phosphatase 1 comprise the SAC silencing network that ensures the correct timing for anaphase onset.
Protein misfolding and aggregation are implicated in many neurodegenerative diseases. One of these diseases is Huntington's, which is caused by increased glutamine-encoding trinucleotide repeats ...within the Huntingtin gene. Like other misfolded proteins, mutated Huntingtin proteins with polyglutamine expansions are prone to aggregation. Misfolded proteins exist as soluble monomers, small aggregates, or as large insoluble inclusion bodies. Misfolded protein aggregates are believed to be cytotoxic by stressing the protein degradation machinery, disrupting membrane structure, or sequestering other proteins. We recently showed that expression of misfolded proteins lowers cellular free ubiquitin levels, which compromises the protein degradation machinery. Therefore, the efficient degradation of misfolded proteins is critical to preserve cell health. Cells employ two major mechanisms to degrade misfolded proteins. The first is the ubiquitin-proteasome system (UPS), which ubiquitinates and degrades misfolded proteins with the assistance of segregase Cdc48/p97. The UPS pathway is mainly responsible for the clearance of misfolded proteins present as monomers or smaller aggregates. The second pathway is macroautophagy/autophagy, in which protein aggregates or inclusion bodies are recruited into an autophagosome before transport to the vacuole/lysosome for degradation. This review is focused on the current understanding of the cytotoxicity of misfolded proteins as well as their clearance pathways, with a particular emphasis on mutant Huntingtin.
Chromosome bipolar attachment is achieved when sister kinetochores are attached by microtubules emanating from opposite spindle poles, and this process is essential for faithful chromosome ...segregation during anaphase. A fundamental question in cell biology is how cells ensure that chromosome segregation only occurs after bipolar attachment. It is well documented that unattached kinetochores activate the spindle assembly checkpoint (SAC) to delay chromosome segregation. Therefore, the silencing of the SAC is thought to trigger anaphase onset, but how correct chromosome attachment is coupled with SAC silencing and the subsequent anaphase onset is poorly understood. The establishment of chromosome bipolar attachment not only results in the occupancy of kinetochores by microtubules but also applies tension on sister kinetochores. A long-standing debate is whether the kinetochore attachment (occupancy) or the tension silences the SAC. Recent work in budding yeast reveals the SAC silencing network SSN that prevents SAC silencing prior to tension generation at kinetochores. Therefore, this signaling pathway ensures that SAC silencing and the subsequent anaphase onset occur only after chromosome bipolar attachment applies tension on chromosomes. This review will summarize the recent advances in the understanding of the SAC silencing process.
Fluoride ion batteries (FIBs) are regarded as promising energy storage devices, and it is important and urgent to develop cathode materials with high energy densities for use in FIBs. However, ...systematic investigations of 3d transition metal/metal fluorides have been rarely reported thus far because of the restricted reversibility and unfavorable interfacial compatibility of 3d transition metal/metal fluorides with solid-state electrolytes. Herein, 3d transition metals are investigated by utilizing thin-film cells with LaF
3
substrates. The highly reversible (de)fluorinations of Cu, Co, and Ni are validated at various temperatures. High capacity utilizations of 79.5%, 100%, and 90.5% are obtained during the initial cycle at 150 °C. By combining results from X-ray absorption spectroscopy (XAS) and electrochemical characterization, the electrochemical behaviors of Cu, Co, and Ni, as well as experimental evidence of the two-phase transition mechanism during the M/MF
2
reaction are reported for the first time. This provides new insights required for future cathode designs for use in all-solid-state FIBs.
Fluoride ion batteries (FIBs) are regarded as promising energy storage devices, and it is important and urgent to develop cathode materials with high energy densities for use in FIBs.
The spindle assembly checkpoint (SAC) prevents anaphase onset in response to chromosome attachment defects, and SAC silencing is essential for anaphase onset. Following anaphase onset, activated ...Cdc14 phosphatase dephosphorylates the substrates of cyclin-dependent kinase to facilitate anaphase progression and mitotic exit. In budding yeast, Cdc14 dephosphorylates Fin1, a regulatory subunit of protein phosphatase 1 (PP1), to enable kinetochore localization of Fin1-PP1. We previously showed that kinetochore-localized Fin1-PP1 promotes the removal of the SAC protein Bub1 from the kinetochore during anaphase. We report here that Fin1-PP1 also promotes kinetochore removal of Bub3, the Bub1 partner, but has no effect on another SAC protein Mad1. Moreover, the kinetochore localization of Bub1-Bub3 during anaphase requires Aurora B/Ipl1 kinase activity. We further showed that Fin1-PP1 facilitates the dephosphorylation of kinetochore protein Ndc80, a known Ipl1 substrate. This dephosphorylation reduces kinetochore association of Bub1-Bub3 during anaphase. In addition, we found that untimely Ndc80 dephosphorylation causes viability loss in response to tensionless chromosome attachments. These results suggest that timely localization of Fin1-PP1 to the kinetochore controls the functional window of SAC and is therefore critical for faithful chromosome segregation.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
All‐solid‐state fluoride‐ion batteries (FIBs) are regarded as promising energy storage devices; however, currently proposed cathodes fail to meet the requirements for practical applications in terms ...of high energy density and high rate capability. Herein, the first use of stable and low‐cost cuprous oxide (Cu2O) as a cathode material for all‐solid‐state FIBs with reversible and fast (de)fluorination behavior is reported. A phase‐transition reaction mechanism involving Cu+/Cu2+ redox for charge compensation is confirmed, using the combination of electrochemical methods and X‐ray absorption spectroscopy. The first discharge capacity is approximately 220 mAh g−1, and fast capacity fading is observed in the first five cycles, which is ascribed to partial structural amorphization. Compared with those of simple metal/metal fluoride systems, the material shows a superior rate capability, with a first discharge capacity of 110 mAh g−1 at 1 C. The rate‐determining step and probable structural evolutions are investigated as well. It is believed that the comprehensive investigations of Cu2O as a cathode material described in this work can lead to an improved understanding of all‐solid‐state FIBs.
The all‐solid‐state fluoride‐ion battery (FIB) is regarded as one of promising candidates for next‐generation batteries. The high rate capability and high capacity of the Cu2O cathode material offer new possibilities for practical applications of all‐solid‐state FIBs, considering the low‐cost, highly commercialized, and chemical stable characteristics of Cu2O materials.
All-solid-state fluoride-ion batteries (FIBs) that use fluoride ions as carrier ions offer a new horizon for next-generation energy storage devices owing to their high specific capacities. Materials ...that utilize topochemical insertion and desorption reactions of fluoride ions have been proposed as cathodes for FIBs; among them, Ruddlesden–Popper-type perovskite-related compounds are promising cathode materials owing to reversible fluoride-ion (de)intercalations with low volume expansion compared to conversion-type cathode materials. Although it is essential to improve the power density of the compounds for practical application, the relationship between the structure and power density is still not clearly understood. In this study, we synthesized chemically fluorinated Ruddlesden–Popper compounds, LaSrMnO4 and apical-site-substituted oxyfluoride Sr2MnO3F, and examined the correlations between their structures and electrochemical properties; Sr2MnO3F showed better power density. Open-circuit voltage measurements, X-ray absorption spectroscopy, and synchrotron X-ray diffraction revealed that electrochemical F– insertion into LaSrMnO4 proceeds via a two-phase reaction with relatively high volume expansion, whereas that into Sr2MnO3F proceeds via a solid-solution reaction with relatively low volume expansion. The substitution of oxygen in the apical sites with fluorine suppressed phase transitions with large volume changes, resulting in improved power density.
Ubiquilin proteins contain a ubiquitin-like domain (UBL) and ubiquitin-associated domain(s) that interact with the proteasome and ubiquitinated substrates, respectively. Previous work established the ...link between ubiquilin mutations and neurodegenerative diseases, but the function of ubiquilin proteins remains elusive. Here we used a misfolded huntingtin exon I containing a 103-polyglutamine expansion (Htt103QP) as a model substrate for the functional study of ubiquilin proteins. We found that yeast ubiquilin mutant (dsk2Δ) is sensitive to Htt103QP overexpression and has a defect in the formation of Htt103QP inclusion bodies. Our evidence further suggests that the UBL domain of Dsk2 is critical for inclusion body formation. Of interest, Dsk2 is dispensable for Htt103QP degradation when Htt103QP is induced for a short time before noticeable inclusion body formation. However, when the inclusion body forms after a long Htt103QP induction, Dsk2 is required for efficient Htt103QP clearance, as well as for autophagy-dependent delivery of Htt103QP into vacuoles (lysosomes). Therefore our data indicate that Dsk2 facilitates vacuole-mediated clearance of misfolded proteins by promoting inclusion body formation. Of importance, the defect of inclusion body formation in dsk2 mutants can be rescued by human ubiquilin 1 or 2, suggesting functional conservation of ubiquilin proteins.
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