This study will provide a fuller account of the functions of sumimasen, one of the expressions used for both apology and thanks in everyday Japanese conversation. In order to accurately explain these functions, it is necessary to carefully observe the different socio-cultural contexts in which this expression occurs. Hence, a database consisting of ten hours of daily conversation was used as the foundation for the study, with these ten hours of talk yielding a total of 44 tokens of sumimasen. This study will also attempt to relate sumimasen to other strategies for expressing apology and gratitude in Japanese and to examine whether certain values of Japanese society may be reflected through the usage of this expression.

The Multiple Functions of

Neurons born in the embryo can undergo a protracted period of maturation lasting well into postnatal life. How gene expression changes are regulated during maturation and whether they can be recapitulated in cultured neurons remains poorly understood. Here, we show that mouse motor neurons exhibit pervasive changes in gene expression and accessibility of associated regulatory regions from embryonic till juvenile age. While motifs of selector transcription factors, ISL1 and LHX3, are enriched in nascent regulatory regions, motifs of NFI factors, activity-dependent factors, and hormone receptors become more prominent in maturation-dependent enhancers. Notably, stem cell-derived motor neurons recapitulate ~40% of the maturation expression program in vitro, with neural activity playing only a modest role as a late-stage modulator. Thus, the genetic maturation program consists of a core hardwired subprogram that is correctly executed in vitro and an extrinsically-controlled subprogram that is dependent on the in vivo context of the maturing organism. 

/pdf/transcriptional-dynamics-of-murine-motor-neuron-maturation-3gl77go1.pdf

Transcriptional dynamics of murine motor neuron maturation in vivo and in vitro

Site-specific histone modifications have long been recognized to play an important role in directing gene transcription in chromatin in biology of health and disease. However, concrete illustration of how different histone modifications in a site-specific manner dictate gene transcription outcomes, as postulated in the influential "Histone code hypothesis", introduced by Allis and colleagues in 2000, has been lacking. In this review, we summarize our latest understanding of the dynamic regulation of gene transcriptional activation, silence, and repression in chromatin that is directed distinctively by histone H3 lysine 27 acetylation, methylation, and crotonylation, respectively. This represents a special example of a long-anticipated verification of the "Histone code hypothesis." 

Distinct Histone H3 Lysine 27 Modifications Dictate Different Outcomes of Gene Transcription.

Light sheet fluorescence microscopy (LSFM) has become a method of choice for live imaging because of its fast acquisition and reduced photobleaching and phototoxicity. Despite the strengths and growing availability of LSFM systems, no generalized LSFM mounting protocol has been adapted for live imaging of post-embryonic stages of C. elegans. A major challenge has been to develop methods to limit animal movement using a mounting media that matches the refractive index of the optical system. Here, we describe a simple mounting and immobilization protocol using a refractive-index matched UV-curable hydrogel within fluorinated ethylene propylene (FEP) tubes for efficient and reliable imaging of larval and adult C. elegans stages.

https://www.frontiersin.org/articles/10.3389/fcell.2022.1012820/pdf

A light sheet fluorescence microscopy protocol for Caenorhabditis elegans larvae and adults

Cyclin-dependent kinase (CDK) sensors have facilitated investigations of the cell cycle in living cells. These genetically encoded fluorescent biosensors change their subcellular location upon activation of CDKs. Activation is primarily regulated by their association with cyclins, which in turn trigger cell-cycle progression. In the absence of CDK activity, cells exit the cell cycle and become quiescent, a key step in stem cell maintenance and cancer cell dormancy. The evolutionary conservation of CDKs has allowed for the rapid development of CDK activity sensors for cell lines and several research organisms, including nematodes, fish, and flies. CDK activity sensors are utilized for their ability to visualize the exact moment of cell-cycle commitment. This has provided a breakthrough in understanding the proliferation-quiescence decision. Further adoption of these biosensors will usher in new discoveries focused on the cell-cycle regulation of development, ageing, and cancer.

CDK activity sensors: genetically encoded ratiometric biosensors for live analysis of the cell cycle.

SUMMARY Chromatin remodeling complexes, such as the SWItching defective/Sucrose Non- Fermenting (SWI/SNF) ATP-dependent chromatin remodeling complex, coordinate metazoan development through broad regulation of chromatin accessibility and transcription, ensuring normal cell cycle control and cellular differentiation in a lineage- specific and temporally restricted manner. Mutations in the structural subunits of chromatin, such as histone subunits, and chromatin regulating factors (CRFs) are associated with a variety of diseases including cancer metastasis, which co-opts cellular invasion programs functioning in healthy cells during development. Here we utilize Caenorhabditis elegans anchor cell (AC) invasion as an in vivo model to identify the suite of chromatin agents and CRFs that promote cellular invasiveness. We demonstrate that the SWI/SNF ATP-dependent chromatin remodeling complex is a critical regulator of AC invasion, with pleiotropic effects on both G0 cell cycle arrest and activation of invasive machinery. Using targeted protein degradation and RNA interference (RNAi), we show that SWI/SNF contributes to AC invasion in a dose-dependent fashion, with lower levels of activity in the AC corresponding to aberrant cell cycle entry and increased loss of invasion. Specifically, we implicate the SWI/SNF BAF assembly in the regulation of the cell cycle, whereas our data suggests that the SWI/SNF PBAF assembly promotes AC attachment to the basement membrane (BM) and promotes the activation of the invasive machinery. Together these findings demonstrate that the SWI/SNF complex is necessary for two essential components of AC invasion: arresting cell cycle progression and remodeling the BM. The work here provides valuable single-cell mechanistic insight into how the SWI/SNF assemblies differentially contribute to cellular invasion and how SWI/SNF subunit-specific disruptions may contribute to tumorigeneses and cancer metastasis. SUMMARY STATEMENT Cellular invasion through the basement membrane by the C. elegans anchor cell requires both BAF and PBAF SWI/SNF assemblies to arrest the cell cycle and promote the expression of pro-invasive genes.

https://www.biorxiv.org/content/biorxiv/early/2021/03/02/2021.03.01.433447.1.full.pdf

The SWI/SNF chromatin remodeling assemblies BAF and PBAF differentially regulate cell cycle exit and cellular invasion in vivo

Spinal motor neurons (MNs) constitute cellular substrates for several movement disorders Although their early development has received much attention, how spinal MNs become and remain terminally differentiated is poorly understood Here, we determined the transcriptome of mouse brachial MNs at embryonic and postnatal stages We found that genes encoding homeodomain (HOX, LIM) transcription factors (TFs), previously implicated in early MN development, continue to be expressed postnatally, suggesting later functions To test this, we inactivated Hoxc8 at successive stages of MN development We found that Hoxc8 is not only required to establish but also maintain expression of several MN terminal differentiation markers Furthermore, we uncovered novel TFs with continuous MN expression, a Hoxc8 dependency for maintained expression of Iroquois (Irx) homeodomain TFs, and a new role for Irx2 in MN development Our findings dovetail recent observations in C elegans MNs, pointing toward an evolutionarily conserved role for Hox in neuronal terminal differentiation

/pdf/control-of-spinal-motor-neuron-terminal-differentiation-moii16mm19.pdf

Control of spinal motor neuron terminal differentiation through sustained Hoxc8 gene activity

Ribosomal RNAs (rRNAs) have long been known to carry modifications, including numerous sites of 2’O-methylation and pseudouridylation, as well as N6-methyladenosine (m6A), and N6,6-dimethyladenosine. While the functions of many of these modifications are unclear, some are highly conserved and occur in regions of the ribosome critical for mRNA decoding. Both 28S rRNA and 18S rRNA carry m6A, and while ZCCHC4 has been identified as the methyltransferase responsible for the 28S rRNA m6A site, the methyltransferase responsible for the 18S rRNA m6A site has remained uncharacterized until recently. Here, we show that the METTL5-TRMT112 complex is the methyltransferase responsible for installing m6A at position 1832 of human 18S rRNA. TRMT112 is required for the metabolic stability of METTL5, and human METTL5 mutations associated with microcephaly and intellectual disability disrupt this interaction. Loss of METTL5 in human cancer lines alters the translation of transcripts associated with mitochondrial biogenesis and function. Mettl5 knockout mice display reduced body size and evidence of metabolic defects. This m6A site is located on the 3’ end of 18S rRNA, which may become surface-exposed under some circumstances and thus may play a regulatory role in translation of specific transcripts. While recent work has focused heavily on m6A modifications in mRNA and its roles in mRNA processing and translation, deorphanizing putative methyltransferase enzymes is revealing previously unappreciated regulatory roles for m6A in noncoding RNAs.

/pdf/the-mettl5-trmt112-n6-methyladenosine-methyltransferase-1ixfngkmug.pdf

The METTL5-TRMT112 N6-methyladenosine methyltransferase complex regulates metabolism and development via translation

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The SWI/SNF chromatin remodeling assemblies BAF and PBAF differentially regulate cell cycle exit and cellular invasion in vivo

Control of spinal motor neuron terminal differentiation through sustained Hoxc8 gene activity

The METTL5-TRMT112 N6-methyladenosine methyltransferase complex regulates metabolism and development via translation