516 research outputs found
Crystal structure of turneaureite and crystal-chemical relationships among the minerals of the svabite subgroup (apatite supergroup)
No full textMinerals of the apatite supergroup have the general formula M12M23(TO4)3X. Within the apatite
supergroup, the triad svabite – johnbaumite – turneaureite represents one of the rare cases in which three
natural end-members are known corresponding to three different X– anions, i.e., svabite, Ca5(AsO4)3F,
johnbaumite, Ca5(AsO4)3(OH), and turneaureite, Ca5(AsO4)3Cl. The only other known case is represented by
the eponymous series of calcium phospates fluorapatite – hydroxylapatite – chlorapatite (Pasero et al., 2010).
We present here the results of a combined chemical (electron microprobe) and structural (single crystal Xray
diffraction) study of turneaureite, which follows similar studies carried out on johnbaumite (Biagioni &
Pasero, 2013) and svabite (Biagioni et al., 2016). This allows us to make a comparative analysis of the
crystal-chemical features of the three calcium arsenate minerals with the apatite structure.
The studied sample of turneaureite comes from Nordmark, Värmland, Sweden. Electron microprobe
analyses resulted in the following empirical formula: (Ca4.82Mn0.17Ba0.02Sr0.01)(As2.94P0.02S0.02Si0.01)O12
[Cl0.47(OH)0.42F0.11]. The crystal structure of turneaureite was refined in the space group P63/m to R1 = 0.0180,
wR2 = 0.0475 for 716 independent reflections, with a = 9.9218(3), c = 6.8638(2) Å.
The crystal structure of turneaureite was compared with those of johbaumite (sample from the
Jakobsberg mine) and of svabite (sample from the Harstigen mine). The samples of all three minerals
originate from three neighbouring Långban-type deposits in the county of Värmland.
The geometry of the coordination polyhedra is similar in these three minerals of the savbite
subgroup. M1Ca atoms are nine-fold coordinated in tri-augmented trigonal prisms, M2Ca2 atoms are sevenfold
coordinated in pentagonal bipyramids, and TAs atoms are tetrahedrally coordinated. Also average bond
distances are quite similar in the three structures (johnbaumite, svabite, turneaureite, in Å: = 2.586,
2.586, 2.579; = 2.480, 2.485, 2.529; = 1.671, 1.674, 1.678). There is, however, a relevant
difference in the z fractional coordinate of X– anionic position (0, 0, z). In turneaureite chlorine lies at z =
0.319, with an additional mixed-occupancy (OH/F/Cl) site at z = 1/4. In johnbaunite the hydroxyl group lies
at z = 0.216, with no additional site. In svabite fluorine lies at z = 1/4, with an additional, mixed-occupancy
(F/OH) site at z = 0.195. This results in different Ca2–X bond distances in the three minerals, in keeping with
the variable nature of the X– anion
Crystal-chemistry of sulfates from the Apuan Alps, Tuscany, Italy. VIII. New data on khademite, Al(SO 4)F(H 2 O) 5
No full textKhademite, ideally Al(SO4)F(H2O)5, from the Monte Arsiccio mine, Apuan Alps, Tuscany, Italy, has been characterised through quantitative electron microprobe analysis, micro-Raman spectroscopy and single-crystal X-ray diffraction. Khademite occurs as colourless to whitish tabular crystals, up to 5 mm. Electron microprobe analysis (in wt.%, average of 20 spot analyses) gave: SO3 35.43, Al2O3 21.27, F 6.92, H2Ocalc 39.73, sum 103.35, -O = F 2.92, total 100.43. On the basis of 10 anions per formula unit, assuming the occurrence of 5 H2O groups and 1 (F+OH) atom per formula unit, its chemical formula can be written as Al0.96S1.02O4[F0.84(OH)0.16]Σ1.00·5H2O. The Raman spectrum of khademite is characterised by the occurrence of vibrational modes of SO4 groups and by broad and strong bands due to the O-H stretching modes. Khademite is orthorhombic, space group Pcab, with unit-cell parameters a = 11.1713(2), b = 13.0432(3), c = 10.8815(2) Å, V = 1585.54(5) Å3 and Z = 8. The crystal structure refinement converged to R1 = 0.0293 on the basis of 2359 unique reflections with Fo > 4σ(Fo) and 152 refined parameters. The crystal structure of khademite is characterised by the alternation, along b, of two distinct kinds of {010} layers, one formed by [001] rows of isolated Al-centred octahedra, connected to each other through H bonds, and the other showing isolated SO4 groups. Along b, oxygen atoms belonging to SO4 groups act as acceptor of H bonds from H2O groups coordinating Al atoms. The new data improved the description of the H bonds in khademite and led us to discuss about the possible existence of its (OH)-analogue, rostite. In addition, Raman spectroscopic data were collected on the same crystal used for the crystal-chemical characterisation, allowing a comparison with previous results
21st Italian Workshop on Neural Networks
No full textWIRN 2011
The Italian Workshop on Neural Networks (WIRN) is the annual conference of the Italian Society of Neural
Networks (SIREN). The conference is organized continuously, since 1989, in co-operation with the
International Institute for Advanced Scientific Studies (IIASS) of Vietri S/M (Italy), and is a traditional event
devoted to the discussion of novelties and innovations related to the Artificial Neural Networks.
The 21st Edition of the Italian Workshop on Neural Networks (WIRN 2011) will be held, as usual, at the
beautiful town of Vietri sul Mare, near Salerno, Italy.
CALL FOR PAPERS, SPECIAL SESSIONS PROPOSALS: Prospective authors are invited to contribute
high quality papers in the topic areas listed below and proposals for special sessions. Special sessions aim to
bring together researchers in special focused topics. Each special session should include at least 3 contributing
papers. A proposal for a special session should include a summary statement (1 page long) describing the
motivation and relevance of the proposed special session, together with the article titles and author names of
the papers that will be included in the track. The co-ordinator of the proposal will also be responsible for the
reviewing procedure.
Contributions should be high quality, original and not published elsewhere or submitted for publication during
the review period. Please visit the web site for further details of the required paper format. Papers will be
reviewed by the Program Committee, and may be accepted for oral or poster presentation. All contributions
will be published in a proceeding volume by IOS Press. Authors will be limited to one paper per registration.
The submission of the manuscripts should be done through the following website (page limit: 8 pages):
https://www.easychair.org/conferences/?conf=wirn2011
SPECIAL SESSION ALREADY FINALIZED: The WIRN 2011 will feature the following three Special
Sessions:
i) Models of Behaviours for Human-Machine Interaction (Chairs: A. Esposito, M. Maldonato, L.
Trojano)
ii) Autonomous Machine Learning (Chairs: A. Roy, P. Arena), in cooperation with INNS SIG AML
iii) Neuromorphic Engineering (Chairs: E. Chicca, e. Pasero)
Contributions are also sought for the Special sessions (see website for additional info
Towards Socially and Emotionally Believable ICT Interfaces
No full textIn order to realize an artificial intelligence focused on human needs, it is necessary to identify the interactional characteristics that describe human mood, social behavior, beliefs, and experiences. The cross-modal analysis of communicative macro-signals represents the first step in this direction. The second step requires the definition of adequate mathematical representations of these signals to validate them perceptively (on the human side) and computationally
Regulation of Mec1 (ATR) signaling in budding yeast
No full textCells are continuously challenged by various sources of DNA damage that can contribute to cancer formation if not appropriately repaired. To cope with this threat, cells have conserved mechanisms called the DNA damage checkpoints that sense damaged DNA, stop the cell cycle, and upregulate DNA repair. Central players in these checkpoints are the PI3K-like kinases ATM and ATR (S.c. Tel1 and Mec1). Mec1 senses single stranded DNA (ssDNA) that is exposed at stalled replication forks and activates the S phase checkpoint. However, ssDNA, which is generated at the lagging strand during normal replication, does not cause detectable checkpoint activation. It is unknown how Mec1 is regulated in S phase. To study this, we took advantage of a mutant allele of MEC1, mec1-100, which is proficient for the G2 DNA damage checkpoint, but is compromised in G1-S and intra-S-phase checkpoints.
In the first part of this thesis we aimed at identifying regulatory factors. We screened for spontaneous survivors on a lethal dose of the replication fork-stalling agent hydroxyurea (HU) for mec1-100 cells. We mapped additional mutations in mec1-100 or mutations in either PPH3 or PSY2, which form a highly conserved phosphatase (PP4) complex. In a second, more unbiased, high-throughput screen we combined mec1-100 with a collection of 1525 gene deletions involved in chromatin processes and scored double mutants for HU sensitivity. pph3Δ and psy2Δ were among the top mec1-100 suppressor hits, confirming a strong genetic interaction. Suppression by pph3Δ was correlated with the phosphorylation of the downstream kinase Rad53. However, it did not depend exclusively on Rad53, because residual suppression of mec1-100 by pph3Δ could also be observed in rad53Δ cells. We tested whether Psy2-Pph3 might regulate Mec1 directly, and found a physical interaction between Psy2 and Ddc2-Mec1. Moreover, we found that a phosphorylation site within Mec1 (S1991) is downregulated in mec1-100 cells and restored when Pph3 is also lost. However, we were unable to demonstrate that Pph3 dephosphorylates Mec1 directly in vitro. Phosphorylation required both Mec1 kinase activity and Rad53. Thus, we speculate that Mec1 phosphorylation is achieved through Rad53, which is in turn regulated by Pph3, indicating the existence of a feedback loop from Rad53 back to Mec1. Mutation of the phosphorylation site renders cells sensitive to the radiomimetic drug Zeocin, indicating an important role in the survival of DNA damage. Finally, we applied quantitative phosphoproteomics to identify Mec1 and Pph3 targets. We found that the levels of the majority of the phosphopeptides that are affected by a tel1Δ mec1-100 mutation but not by rad53Δ can be rescued due to additional deletion of PPH3. The data presented here support a model in which Pph3 is a major regulator of Mec1 signaling.
In a second part mec1-100 was further characterized in order to understand the mechanism by which its two point mutations outside of the catalytic domain (F1179S, N1700S) cause defects in the replication checkpoint. We find that the mutations leave kinase activity in vitro, oligomerization and Ddc2-Mec1 interaction intact. Genetic analysis shows that mec1-100 is additive, rather than epistatic with mutation or deletion of any of the canonical checkpoint activating proteins Ddc1, Dna2, Dpb11, Rad24, Mrc1, Rad9, Tel1 or Chk1. Thus, we conclude that mec1-100 does not impair function of any of these proteins. We hypothesized that the mutated region might constitute a regulatory domain that is bound by a yet unknown factor. IP experiments followed by mass spectrometry analysis did not show reproducibly decreased interaction of any protein. Additional detailed biochemical analysis is needed to fully understand the mechanism of the two mec1-100 mutations.
We further characterize intragenic mec1-100 suppressor mutations by mapping them to a homology model. While some mutations reside within the kinase domain, and could influence catalytic activity, others might as well be involved protein-protein interactions. We asked whether suppression would involve Rad24 dependent Mec1 activation. Interestingly, we find that suppression by mutations in residues that might make protein-protein contacts completely requires Rad24. Other suppressor mutations relied less on Rad24. Thus, we conclude that intragenic suppression of mec1-100 HU sensitivity employs at least two different mechanisms: one that is Rad24-dependent and a second that is Rad24–independent. These unpublished results will help in understanding Mec1 function and regulation once structural data is available.
The third experimental part resolves the role of the RecQ helicase Sgs1 in replication checkpoint signaling. It was shown before that Sgs1 and Mec1 synergistically contribute to replication fork stabilization under replication stress. Both interact with the ssDNA binding protein RPA. Here, we created a mutant, sgs1-r1, which lacks the RPA interaction domain. While sgs1-r1 is proficient to stabilize stalled forks under replication stress, it is synthetic lethal with mus81Δ, slx4Δ, slx5Δ and slx8Δ. These could provide alternative means to recover stalled forks by resolving crossover structures, DNA repair or break induced replication. . Sgs1 was previously shown to promote Rad53 activation in a manner independent of its helicase activity. We show here that Sgs1 checkpoint function requires the R1 domain. Mec1 phosphorylates Sgs1 in this domain and Sgs1 phosphorylation allows its binding to Rad53 in vitro and in vivo. We thus propose that Sgs1 serves as a mediator in checkpoint signaling by recruiting Rad53 to stalled replication forks for activation.
This work provides new insights into Mec1 signaling by elucidating the checkpoint function of Sgs1 and defining Psy2-Pph3 as a major regulator of this pathway
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