Astrin is required for the maintenance of sister chromatid cohesion and centrosome integrity

Faithful chromosome segregation in mitosis requires the formation of a bipolar mitotic spindle with stably attached chromosomes. Once all of the chromosomes are aligned, the connection between the sister chromatids is severed by the cysteine protease separase. Separase also promotes centriole disengagement at the end of mitosis. Temporal coordination of these two activities with the rest of the cell cycle is required for the successful completion of mitosis. In this study, we report that depletion of the microtubule and kinetochore protein astrin results in checkpoint-arrested cells with multipolar spindles and separated sister chromatids, which is consistent with untimely separase activation. Supporting this idea, astrin-depleted cells contain active separase, and separase depletion suppresses the premature sister chromatid separation and centriole disengagement in these cells. We suggest that astrin contributes to the regulatory network that controls separase activity

Unified description of Fermi and non-Fermi liquid behavior in a conserving slave boson approximation for strongly correlated impurity models

We show that the presence of Fermi or non-Fermi liquid behavior in the SU(N) x SU(M) Anderson impurity models may be read off the infrared threshold exponents governing the spinon and holon dynamics in a slave boson representation of these models. We construct a conserving T-matrix approximation which recovers the exact exponents with good numerical accuracy. Our approximation includes both coherent spin flip scattering and charge fluctuation processes. For the single-channel case the tendency to form bound states drastically modifies the low energy behavior. For the multi-channel case in the Kondo limit the bound state contributions are unimportant.Comment: 4 pages, Latex, 3 postscript figures included Final version with minor changes in wording, to appear in Phys.Rev.Let

Evaluation of the American yam bean (Pachyrhizus spp.) for storage root yield across varying eco-geographic conditions in Uganda

Open Access Article; Published online: 15 June 2019The American yam bean (Pachyrhizus spp.) is a legume crop that is exclusively used for its storage roots. The seeds are inedible due to presence of toxic rotenone. It produces high storage root yields comparable of major root crops like cassava or sweetpotato. And flower pruning more than doubles its root yield performance. Using twenty five yam bean accessions, the current study aimed to determine root yield stability and adaptability, and presence of yam bean production mega environments in Uganda. Trials were planted at three stations, Namulonge, Serere, and Kachwekano during two consecutive seasons of 2011. Fresh storage root yields were significantly different (p < 0.05) across locations with the ideal location being Namulonge (fresh storage root yield of 10.1 t ha-1), followed by Serere (8.0 t ha-1), and Kachwekano (3.1 t ha-1). Results of AMMI analysis indicated the presence of genotype-by-environment interaction for fresh storage root yield. Through AMMI estimates and GGE visual assessment, genotype 209017 was the highest yielding with mean yield of 20.7 t ha-1. Genotype 209018 with mean yield of 15.5 t ha-1 was the most stable and adapted accession in the entire discriminating environment in Uganda. From the environmental focusing plot, the six environments were grouped into two putative mega environments for yam bean production

Unusual misregulation of RNA splicing caused by insertion of a transposable element into the T (Brachyury) locus

BACKGROUND: The T(Wis )mutant allele of the Brachyury, or T, gene was created by insertion of an endogenous retrovirus-like early transposon (ETn) element into the exon 7 splice donor consensus sequence of the 8 exon T locus. While the developmental consequences of this disruption have been well characterized, the molecular consequences have not been previously investigated, and it has been assumed that the insertion results in a truncated protein. This study sought to further characterize the mutant T(Wis )allele by investigating the nature of the transcripts produced by insertion of this transposable element. RESULTS: Using an RT-PCR based approach, we have shown that at least 8 different mutant transcripts are produced from the T(Wis )allele. All T(Wis )transcripts bypass the mutated exon 7 splice donor site, such that wild type T transcripts are not produced from the T(Wis )allele. CONCLUSIONS: This result shows an unsuspected misregulation of RNA splicing caused by insertion of a transposable element, that could have more widespread consequences in the genome

Mejorando agricultura, mejorando nutrición.

PCCMCA. LEG 47

Longitudinal Evaluation of an N-Ethyl-N-Nitrosourea-Created Murine Model with Normal Pressure Hydrocephalus

Normal-pressure hydrocephalus (NPH) is a neurodegenerative disorder that usually occurs late in adult life. Clinically, the cardinal features include gait disturbances, urinary incontinence, and cognitive decline.Herein we report the characterization of a novel mouse model of NPH (designated p23-ST1), created by N-ethyl-N-nitrosourea (ENU)-induced mutagenesis. The ventricular size in the brain was measured by 3-dimensional micro-magnetic resonance imaging (3D-MRI) and was found to be enlarged. Intracranial pressure was measured and was found to fall within a normal range. A histological assessment and tracer flow study revealed that the cerebral spinal fluid (CSF) pathway of p23-ST1 mice was normal without obstruction. Motor functions were assessed using a rotarod apparatus and a CatWalk gait automatic analyzer. Mutant mice showed poor rotarod performance and gait disturbances. Cognitive function was evaluated using auditory fear-conditioned responses with the mutant displaying both short- and long-term memory deficits. With an increase in urination frequency and volume, the mutant showed features of incontinence. Nissl substance staining and cell-type-specific markers were used to examine the brain pathology. These studies revealed concurrent glial activation and neuronal loss in the periventricular regions of mutant animals. In particular, chronically activated microglia were found in septal areas at a relatively young age, implying that microglial activation might contribute to the pathogenesis of NPH. These defects were transmitted in an autosomal dominant mode with reduced penetrance. Using a whole-genome scan employing 287 single-nucleotide polymorphic (SNP) markers and further refinement using six additional SNP markers and four microsatellite markers, the causative mutation was mapped to a 5.3-cM region on chromosome 4.Our results collectively demonstrate that the p23-ST1 mouse is a novel mouse model of human NPH. Clinical observations suggest that dysfunctions and alterations in the brains of patients with NPH might occur much earlier than the appearance of clinical signs. p23-ST1 mice provide a unique opportunity to characterize molecular changes and the pathogenic mechanism of NPH

Recruitment of the mitotic exit network to yeast centrosomes couples septin displacement to actomyosin constriction

The Mitotic Exit Network (MEN) promotes mitotic exit and cytokinesis but if and how MEN independently controls these two processes is unclear. Here, the authors report that MEN displaces septins from the cell division site to promote actomyosin ring constriction, independently of MEN control of mitotic exit