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Restricting ribosome biosynthesis and assembly in response to nutrient starvation is a universal phenomenon that enables cells to survive with limited intracellular resources. When cells experience starvation, nutrient signaling pathways, such as the target of rapamycin (TOR) and protein kinase A (PKA), become quiescent, leading to several transcription factors and histone modification enzymes cooperatively and rapidly repressing ribosomal genes. Fission yeast has factors for heterochromatin formation similar to mammalian cells, such as H3K9 methyltransferase and HP1 protein, which are absent in budding yeast. However, limited studies on heterochromatinization in ribosomal genes have been conducted on fission yeast. Herein, we shed light on and compare the regulatory mechanisms of ribosomal gene transcription in two species with the latest insights. [ABSTRACT FROM AUTHOR]

Centromeres are established by nucleosomes containing the histone H3 variant CENP-A. CENP-A is recruited to centromeres by the Mis18–HJURP machinery. During mitosis, CENP-A recruitment ceases, implying the necessity of CENP-A maintenance at centromeres, although the exact underlying mechanism remains elusive. Herein, we show that the inner kinetochore protein Mis6 (CENP-I) and Mis15 (CENP-N) retain CENP-A during mitosis in fission yeast. Eliminating Mis6 or Mis15 during mitosis caused immediate loss of pre-existing CENP-A at centromeres. CENP-A loss occurred due to the transcriptional upregulation of non-coding RNAs at the central core region of centromeres, as confirmed by the observation RNA polymerase II inhibition preventing CENP-A loss from centromeres in the mis6 mutant. Thus, we concluded that the inner kinetochore complex containing Mis6–Mis15 blocks the indiscriminate transcription of non-coding RNAs at the core centromere, thereby retaining the epigenetic inheritance of CENP-A during mitosis. The kinetochore protein Mis6 (CENP-I) plays an important role in CENP-A maintenance during mitosis in fission yeast and blocks the indiscriminate transcription of non-coding RNAs at the core centromere to retain CENP-A during mitosis. [ABSTRACT FROM AUTHOR]

Dressed states were proposed to define the infrared (IR) finite S-matrix in QED or gravity. We show that the original Kulish-Faddeev dressed states are not enough to cure the IR divergences. To illustrate this problem, we consider QED with background currents (Wilson lines). This theory is exactly solvable but shares the same IR problems as the full QED. We show that naive asymptotic states lead to IR divergences in the S-matrix and are also inconsistent with the asymptotic symmetry, even if we add the original Kulish-Faddeev dressing operators. We then propose new dressed states which are consistent with the asymptotic symmetry. We show that the S-matrix for the dressed states is IR finite. We finally conclude that appropriate dressed asymptotic states define the IR finite S-matrix in the full QED. [ABSTRACT FROM AUTHOR]

We first show that a class of operators acting on a given bipartite pure state on ℋA ⊗ ℋB can shrink its supports on ℋA ⊗ ℋB to only ℋA or ℋB while keeping its mappings. Using this result, we show how to systematically construct the decoders of the quantum error-correcting codes against erasure errors. The implications of the results for the operator dictionary in the AdS/CFT correspondence are also discussed. The "sub- algebra code with complementary recovery" introduced in the recent work of Harlow is a quantum error-correcting code that shares many common features with the AdS/CFT correspondence. We consider it under the restriction of the bulk (logical) Hilbert space to a subspace that generally has no tensor factorization into subsystems. In this code, the central operators of the reconstructed algebra on the boundary subregion can emerge as a consequence of the restriction of the bulk Hilbert space. Finally, we show a theorem in this code which implies the validity of not only the entanglement wedge reconstruction but also its converse statement with the central operators. [ABSTRACT FROM AUTHOR]

Microtubules play multiple roles in a wide range of cellular phenomena, including cell polarity establishment and chromosome segregation. A number of microtubule regulators have been identified, including microtubule-associated proteins and kinases, and knowledge of these factors has contributed to our molecular understanding of microtubule regulation of each relevant cellular process. The known regulators, however, are insufficient to explain how those processes are linked to one another, underscoring the need to identify additional regulators. To find such novel mechanisms and microtubule regulators, we performed a screen that combined genetics and microscopy for fission yeast mutants defective in microtubule organization. We isolated approximately 900 mutants showing defects in either microtubule organization or the nuclear envelope, and these mutants were classified into 12 categories. We particularly focused on one mutant, kis1, which displayed spindle defects in early mitosis. The kis1 mutant frequently failed to assemble a normal bipolar spindle. The responsible gene encoded a kinetochore protein, Mis19 (also known as Eic1), which localized to the interface of kinetochores and spindle poles. We also found that the inner kinetochore proteins Mis6/CENP-I and Cnp1/CENP-A were delocalized from kinetochores in the kis1 cells and that kinetochore-microtubule attachment was defective. Another mutant, mis6, also displayed similar spindle defects. We conclude that Kis1 is required for inner kinetochore organization, through which Kis1 ensures kinetochore-microtubule attachment and spindle integrity. Thus, we propose an unexpected relationship between inner kinetochore organization and spindle integrity. [ABSTRACT FROM AUTHOR]

Phenotypic variation occurs through genome rearrangements and mutations in certain responsible genes; however, systematic gene identification methodologies based on genome rearrangements have not been fully established. Here, we explored the loci responsible for the given phenotype using the TAQing system and compared it with a conventional mutagenesis-based method. Two yeast strains with different genetic backgrounds and flocculation phenotypes were fused and genomic rearrangements were induced by transient DNA breaks. Then, selection pressure was applied and multiple mutants were generated, showing different flocculation abilities. We also raised mutants with altered cohesiveness due to spontaneous mutations during long-term recursive passages of haploid strains without TAQing treatment. Comparative genomic analysis of the TAQed mutants revealed three chromosomal regions harboring pivotal flocculation genes, whereas conventional mutagenesis generated a more diverse list of candidate loci after prolonged selection. The combined use of these approaches will accelerate the identification of genes involved in complex phenotypes. [ABSTRACT FROM AUTHOR]

Target of rapamycin complex 1 (TORC1) is activated in response to nutrient availability and growth factors, promoting cellular anabolism and proliferation. To explore the mechanism of TORC1-mediated proliferation control, we performed a genetic screen in fission yeast and identified Sfp1, a zinc-finger transcription factor, as a multicopy suppressor of temperature-sensitive TORC1 mutants. Our observations suggest that TORC1 phosphorylates Sfp1 and protects Sfp1 from proteasomal degradation. Transcription analysis revealed that Sfp1 positively regulates genes involved in ribosome production together with two additional transcription factors, Ifh1/Crf1 and Fhl1. Ifh1 physically interacts with Fhl1, and the nuclear localization of Ifh1 is regulated in response to nutrient levels in a manner dependent on TORC1 and Sfp1. Taken together, our data suggest that the transcriptional regulation of the genes involved in ribosome biosynthesis by Sfp1, Ifh1, and Fhl1 is one of the key pathways through which nutrient-activated TORC1 promotes cell proliferation. [ABSTRACT FROM AUTHOR]