Layered Cost-Map-Based Traffic Management for Multiple Automated Mobile Robots via a Data Distribution Service

This letter proposes traffic management for multiple automated mobile robots (AMRs) based on a layered cost map. Multiple AMRs communicate via a data distribution service (DDS), which is shared by topics in the same DDS domain. The cost of each layer is manipulated by topics. The traffic management server in the domain sends or receives topics to each of AMRs. Using the layered cost map, the new concept of prohibition filter, lane filter, fleet layer, and region filter are proposed and implemented. The prohibition filter can help a user set an area that would prohibit an AMR from trespassing. The lane filter can help set one-way directions based on an angle image. The fleet layer can help AMRs share their locations via the traffic management server. The region filter requests for or receives an exclusive area, which can be occupied by only one AMR, from the traffic management server. All the layers are experimentally validated with real-world AMRs. Each area can be configured with user-defined images or text-based parameter files.Comment: 8 pages, 13 figure

Loss of muscleblind-like 1 results in cardiac pathology and persistence of embryonic splice isoforms.

Cardiac dysfunction is a prominent cause of mortality in myotonic dystrophy I (DM1), a disease where expanded CUG repeats bind and disable the muscleblind-like family of splice regulators. Deletion of muscleblind-like 1 (Mbnl1(ΔE2/ΔE2)) in 129 sv mice results in QRS, QTc widening, bundle block and STc narrowing at 2-4 months of age. With time, cardiac function deteriorates further and at 6 months, decreased R wave amplitudes, sinus node dysfunction, cardiac hypertrophy, interstitial fibrosis, multi-focal myocardial fiber death and calcification manifest. Sudden death, where no end point illness is overt, is observed at a median age of 6.5 and 4.8 months in ~67% and ~86% of male and female Mbnl1(ΔE2/ΔE2) mice, respectively. Mbnl1 depletion results in the persistence of embryonic splice isoforms in a network of cardiac RNAs, some of which have been previously implicated in DM1, regulating sodium and calcium currents, Scn5a, Junctin, Junctate, Atp2a1, Atp11a, Cacna1s, Ryr2, intra and inter cellular transport, Clta, Stx2, Tjp1, cell survival, Capn3, Sirt2, Csda, sarcomere and cytoskeleton organization and function, Trim55, Mapt, Pdlim3, Pdlim5, Sorbs1, Sorbs2, Fhod1, Spag9 and structural components of the sarcomere, Myom1, Tnnt2, Zasp. Thus this study supports a key role for Mbnl1 loss in the initiation of DM1 cardiac disease

Muscleblind-like 3 deficit results in a spectrum of age-associated pathologies observed in myotonic dystrophy.

Myotonic dystrophy type I (DM1) exhibits distinctive disease specific phenotypes and the accelerated onset of a spectrum of age-associated pathologies. In DM1, dominant effects of expanded CUG repeats result in part from the inactivation of the muscleblind-like (MBNL) proteins. To test the role of MBNL3, we deleted Mbnl3 exon 2 (Mbnl3(ΔE2)) in mice and examined the onset of age-associated diseases over 4 to 13 months of age. Accelerated onset of glucose intolerance with elevated insulin levels, cardiac systole deficits, left ventricle hypertrophy, a predictor of a later onset of heart failure and the development of subcapsular and cortical cataracts is observed in Mbnl3(ΔE2) mice. Retention of embryonic splice isoforms in adult organs, a prominent defect in DM1, is not observed in multiple RNAs including the Insulin Receptor (Insr), Cardiac Troponin T (Tnnt2), Lim Domain Binding 3 (Ldb3) RNAs in Mbnl3(ΔE2) mice. Although rare DM1-like splice errors underlying the observed phenotypes cannot be excluded, our data in conjunction with the reported absence of alternative splice errors in embryonic muscles of a similar Mbnl3(ΔE2) mouse by RNA-seq studies, suggest that mechanisms distinct from the adult retention of embryonic splice patterns may make important contributions to the onset of age-associated pathologies in DM1

Histone variant H3.3 stimulates HSP70 transcription through cooperation with HP1γ

Histone variant H3.3 and heterochromatin protein 1γ (HP1γ) are two functional components of chromatin with role in gene transcription. However, the regulations of their dynamics during transcriptional activation and the molecular mechanisms underlying their actions remain poorly understood. Here, we provide evidence that heat shock-induced transcription of the human HSP70 gene is regulated via the coordinated and interdependent action of H3.3 and HP1γ. H3.3 and HP1γ are rapidly co-enriched at the human HSP70 promoters upon heat shock in a manner that closely parallels the initiation of transcription. Knockdown of H3.3 prevents the stable recruitment of HP1γ, inhibits active histone modifications, and attenuates HSP70 promoter activity. Likewise, knockdown of HP1γ leads to the decreased levels of H3.3 in the promoter regions and the repression of HSP70 genes. HP1γ selectively recognizes particular modification states of H3.3 in the nucleosome for its action. Moreover, HP1γ is overexpressed in three representative cancer cell lines, and its knockdown leads to reduction in HSP70 gene transcription and inhibition of cancer cell proliferation. We conclude that the physical and functional interactions between H3.3 and HP1γ make a unique contribution to acute HSP70 transcription and cancer development related to the misregulation of this transcription event

Selective requirement of H2B N-Terminal tail for p14ARF-induced chromatin silencing

The N-terminal tail of histone H2B is believed to be involved in gene silencing, but how it exerts its function remains elusive. Here, we report the biochemical characterization of p14ARF tumor suppressor as a transcriptional repressor that selectively recognizes the unacetylated H2B tails on nucleosomes. The p14ARF–H2B tail interaction is functional, as the antagonistic effect of p14ARF on chromatin transcription is lost upon deletion or acetylation of H2B tails. Gene expression profiling and chromatin immunoprecipitation studies emphasize the significance of H2B deacetylation and p14ARF recruitment in establishing a repressive environment over the cell cycle regulatory genes. Moreover, HDAC1-mediated H2B deacetylation, especially at K20, constitutes an essential step in tethering p14ARF near target promoters. Our results thus reveal a hitherto unknown role of p14ARF in the regulation of chromatin transcription, as well as molecular mechanisms governing the repressive action of p14ARF

Hepatocyte growth factor induces proliferation of lens epithelial cells through activation of ERK1/2 and JNK/SAPK

PURPOSE. Posterior capsule opacification (PCO) is caused by proliferation and migration of lens epithelial cells (LECs) remaining after cataract surgery. In this study, the effect of HGF in LECs and the signaling pathways that contribute to HGFinduced proliferation were investigated. METHODS. Capsular bags prepared from porcine eyes were maintained in serum-free DMEM. The human lens epithelial B3 cells (HLE B3) and rat lens epithelial explants were cultured in MEM supplemented with 20% FCS and medium 199 with 0.1% BSA, respectively. Cell proliferation was determined by MTT assay, proliferating cell nuclear antigen (PCNA) expression, or flow cytometry. An antisense oligonucleotide was used to inhibit cyclin D1 expression. Activation of the mitogen activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways was detected by immunoblot analysis. RESULTS. The proliferation of LECs in a capsular bag culture was significantly inhibited by treatment with the neutralizing antibody for HGF receptor. Stimulation of HLE B3 with hepatocyte growth factor (HGF) activated the MAPKs, ERK, and JNK/ SAPK, but not p38. Activation of both ERK and JNK/SAPK was necessary for the HGF-stimulated induction of cyclin D1, which in turn was necessary for the HGF-induced proliferation of LECs. PI3K also participated in the regulation of cyclin D1 expression upstream of ERK and JNK/SAPK. CONCLUSIONS. The data indicate that HGF is a potent growth factor for LECs and may contribute to the development of PCO and suggest that the signaling pathways involved in HGF-stimulated proliferation may constitute potential therapeutic targets in the treatment of PCO. (Invest Ophthalmol Vis Sci

Layered-Cost-Map-Based Traffic Management for Multiple AMRs via a DDS

A traffic management system can be used to control multiple automated mobile robots (AMRs) effectively. This paper proposes traffic management for multiple AMRs based on a layered cost map in ROS 2 for multiple purposes. Using the layered cost map, the new concepts of a prohibition filter, lane filter, fleet layer, and region filter are proposed and implemented. The prohibition filter can help a user set an area that would prohibit an AMR from trespassing. The lane filter can help set one-way directions based on an angle image. The fleet layer can help AMRs share their locations via the traffic management server. The region filter requests for or receives an exclusive area, which can be occupied by only one AMR from the traffic management server. Multiple AMRs communicate via a data distribution service (DDS), which is shared by topics in the same DDS domain. The traffic management server in the domain sends or receives topics to each of the AMRs. The experiments of AMRs under the proposed traffic management show the effectiveness of our approach

Linker Histone H1.2 Cooperates with Cul4A and PAF1 to Drive H4K31 Ubiquitylation-Mediated Transactivation

Increasing evidence suggests that linker histone H1 can influence distinct cellular processes by acting as a gene-specific regulator. However, the mechanistic basis underlying such H1 specificity and whether H1 acts in concert with other chromatin-altering activities remain unclear. Here, we show that one of the H1 subtypes, H1.2, stably interacts with Cul4A E3 ubiquitin ligase and PAF1 elongation complexes and that such interaction potentiates target gene transcription via induction of H4K31ubiquitylation, H3K4me3, and H3K79me2. H1.2, Cul4A, and PAF1 are functionally cooperative because their individual knockdown results in the loss of the corresponding histone marks and the deficiency of target gene transcription. H1.2 interacts with the serine 2-phosphorylated form of RNAPII, and we argue that it recruits the Cul4A and PAF1 complexes to target genes by bridging the interaction between the Cul4A and PAF1 complexes. These data define an expanded role for H1 in regulating gene transcription and illustrate its dependence on the elongation competence of RNAPII