Absence Of Lamin Research Articles

Mouse polyomavirus infection induces lamin reorganisation.

The nuclear lamina is a dense network of intermediate filaments beneath the inner nuclear membrane. Composed of A-type lamins (lamin A/C) and B-type lamins (lamins B1 and B2), the nuclear lamina provides a scaffold for the nuclear envelope and chromatin, thereby maintaining the structural integrity of the nucleus. A-type lamins are also found inside the nucleus where they interact with chromatin and participate in gene regulation. Viruses replicating in the cell nucleus have to overcome the nuclear envelope during the initial phase of infection and during the nuclear egress of viral progeny. Here, we focused on the role of lamins in the replication cycle of a dsDNA virus, mouse polyomavirus. We detected accumulation of the major capsid protein VP1 at the nuclear periphery, defects in nuclear lamina staining and different lamin A/C phosphorylation patterns in the late phase of mouse polyomavirus infection, but the nuclear envelope remained intact. An absence of lamin A/C did not affect the formation of replication complexes but did slow virus propagation. Based on our findings, we propose that the nuclear lamina is a scaffold for replication complex formation and that lamin A/C has a crucial role in the early phases of infection with mouse polyomavirus.

Uip4p modulates nuclear pore complex function in Saccharomyces cerevisiae

ABSTRACT A double membrane bilayer perforated by nuclear pore complexes (NPCs) governs the shape of the nucleus, the prominent distinguishing organelle of a eukaryotic cell. Despite the absence of lamins in yeasts, the nuclear morphology is stably maintained and shape changes occur in a regulated fashion. In a quest to identify factors that contribute to regulation of nuclear shape and function in Saccharomyces cerevisiae, we used a fluorescence imaging based approach. Here we report the identification of a novel protein, Uip4p, that is required for regulation of nuclear morphology. Loss of Uip4 compromises NPC function and loss of nuclear envelope (NE) integrity. Our localization studies show that Uip4 localizes to the NE and endoplasmic reticulum (ER) network. Furthermore, we demonstrate that the localization and expression of Uip4 is regulated during growth, which is crucial for NPC distribution.

Lamin A/C Assembly Defects in LMNA-Congenital Muscular Dystrophy Is Responsible for the Increased Severity of the Disease Compared with Emery–Dreifuss Muscular Dystrophy

LMNA encodes for Lamin A/C, type V intermediate filaments that polymerize under the inner nuclear membrane to form the nuclear lamina. A small fraction of Lamin A/C, less polymerized, is also found in the nucleoplasm. Lamin A/C functions include roles in nuclear resistance to mechanical stress and gene regulation. LMNA mutations are responsible for a wide variety of pathologies, including Emery–Dreifuss (EDMD) and LMNA-related congenital muscular dystrophies (L-CMD) without clear genotype–phenotype correlations. Both diseases presented with striated muscle disorders although L-CMD symptoms appear much earlier and are more severe. Seeking for pathomechanical differences to explain the severity of L-CMD mutations, we performed an in silico analysis of the UMD-LMNA database and found that L-CMD mutations mainly affect residues involved in Lamin dimer and tetramer stability. In line with this, we found increased nucleoplasmic Lamin A/C in L-CMD patient fibroblasts and mouse myoblasts compared to the control and EDMD. L-CMD myoblasts show differentiation defects linked to their inability to upregulate muscle specific nuclear envelope (NE) proteins expression. NE proteins were mislocalized, leading to misshapen nuclei. We conclude that these defects are due to both the absence of Lamin A/C from the nuclear lamina and its maintenance in the nucleoplasm of myotubes.

Lamin A/C augments Th1 differentiation and response against vaccinia virus and Leishmania major

Differentiation of naive CD4+ T-cells into functionally distinct T helper (Th) subsets is critical to immunity against pathogen infection. Little is known about the role of signals emanating from the nuclear envelope for T-cell differentiation. The nuclear envelope protein lamin A/C is induced in naive CD4+ T-cells upon antigen recognition and acts as a link between the nucleus and the plasma membrane during T-cell activation. Here we demonstrate that the absence of lamin A/C in naive T-cell reduces Th1 differentiation without affecting Th2 differentiation in vitro and in vivo. Moreover, Rag1−/− mice reconstituted with Lmna−/−CD4+CD25− T-cells and infected with vaccinia virus show weaker Th1 responses and viral removal than mice reconstituted with wild-type T-cells. Th1 responses and pathogen clearance upon Leishmania major infection were similarly diminished in mice lacking lamin A/C in the complete immune system or selectively in T-cells. Lamin A/C mediates Th1 polarization by a mechanism involving T-bet and IFNγ production. Our results reveal a novel role for lamin A/C as key regulator of Th1 differentiation in response to viral and intracellular parasite infections.

Endothelial Nuclear Lamina in Mechanotransduction Under Shear Stress.

Endothelial cells that line the lumen of blood vessels are at the interface between hemodynamic forces and vascular wall biology. Endothelial cells transduce mechanical and biological signals from blood flow into intracellular signaling cascades through a process called mechanotransduction. Mechanotransduction is an important part of normal cell functions, as well as endothelial dysfunction which leads to inflammation and pathological conditions. For example, atherosclerosis preferentially develops in regions of disturbed fluid flow and low shear stress. The nuclear lamina, which sits underneath the nuclear envelope, serves to maintain the nuclear structure while acting as a scaffold for heterochromatin and many transcriptional proteins. Defects in lamina and its associated proteins cause a variety of human diseases including accelerated aging diseases such as Hutchinson-Gilford Progeria syndrome. The role of nuclear lamina in endothelial mechanotransduction, specifically how nuclear mechanics impact gene regulation under shear stress, is not fully understood. In one study, lamin A/C was silenced in bovine aortic endothelial cells to determine its role in both glucocorticoid receptor (GR) nuclear translocation and glucocorticoid response element (GRE) transcriptional activation in response to its natural ligand dexamethasone as well as fluid shear stress. Results suggest that absence of lamin A/C does not hinder passage of GR into the nucleus but nuclear lamina is important to properly regulate GRE transcription. Ongoing research continues to investigate how nuclear lamins contribute to endothelial mechanotransduction and to better understand the role of Lamin A in vascular aging and in the progression of cardiovascular diseases.

Hydroclimate of the Last Glacial Maximum and deglaciation in southern Australia's arid margin interpreted from speleothem records (23–15 ka)

Abstract. Terrestrial data spanning the Last Glacial Maximum (LGM) and deglaciation from the southern Australian region are sparse and limited to discontinuous sedimentological and geomorphological records with relatively large chronological uncertainties. This dearth of records has hindered a critical assessment of the role of the Southern Hemisphere mid-latitude westerly winds on the region's climate during this time period. In this study, two precisely dated speleothem records for Mairs Cave, Flinders Ranges, are presented, providing for the first time a detailed terrestrial hydroclimatic record for the southern Australian drylands during 23–15 ka. Recharge to Mairs Cave is interpreted from the speleothem record by the activation of growth, physical flood layering, and δ18O and δ13C minima. Periods of lowered recharge are indicated by 18O and 13C enrichment, primarily affecting δ18O, argued to be driven by evaporation of shallow soil/epikarst water in this water-limited environment. A hydrological driver is supported by calcite fabric changes. These include the presence of laminae, visible organic colloids, and occasional dissolution features, related to recharge, as well as the presence of sediment bands representing cave floor flooding. A shift to slower-growing, more compact calcite and an absence of lamination is interpreted to represent reduced recharge. The Mairs Cave record indicates that the Flinders Ranges were relatively wet during the LGM and early deglaciation, particularly over the interval 18.9–15.8 ka. This wetter phase ended abruptly with a shift to drier conditions at 15.8 ka. These findings are in agreement with the geomorphic archives for this region, as well as the timing of events in records from the broader Australasian region. The recharge phases identified in the Mairs Cave record are correlated with, but antiphase to, the position of the westerly winds interpreted from marine core MD03-2611, located 550 km south of Mairs Cave in the Murray Canyons region. The implication is that the mid-latitude westerlies are located further south during the period of enhanced recharge in the Mairs Cave record (18.9–16 ka) and conversely are located further north when greater aridity is interpreted in the speleothem record. A further comparison with speleothem records from the northern Australasian region reveals that the availability of tropical moisture is the most likely explanation driving enhanced recharge, with further amplification of recharge occurring during the early half of Heinrich Stadial 1 (HS1), possibly influenced by a more southerly displaced Intertropical Convergence Zone (ITCZ). A rapid transition to aridity at 15.8 ka is consistent with a retraction of this tropical moisture source.

Lamins position the nuclear pores and centrosomes by modulating dynein.

Lamins, the type V nuclear intermediate filament proteins, are reported to function in both interphase and mitosis. For example, lamin deletion in various cell types can lead to an uneven distribution of the nuclear pore complexes (NPCs) in the interphase nuclear envelope, whereas deletion of B-type lamins results in spindle orientation defects in mitotic neural progenitor cells. How lamins regulate these functions is unknown. Using mouse cells deleted of different combinations or all lamins, we show that lamins are required to prevent the aggregation of NPCs in the nuclear envelope near centrosomes in late G2 and prophase. This asymmetric NPC distribution in the absence of lamins is caused by dynein forces acting on NPCs via the dynein adaptor BICD2. We further show that asymmetric NPC distribution upon lamin depletion disrupts the distribution of BICD2 and p150 dynactin on the nuclear envelope at prophase, which results in inefficient dynein-driven centrosome separation during prophase. Therefore lamins regulate microtubule-based motor forces in vivo to ensure proper NPC distribution in interphase and centrosome separation in the mitotic prophase.

Lamin A/C-dependent interaction with 53BP1 promotes cellular responses to DNA damage.

Lamins A/C have been implicated in DNA damage response pathways. We show that the DNA repair protein 53BP1 is a lamin A/C binding protein. In undamaged human dermal fibroblasts (HDF), 53BP1 is a nucleoskeleton protein. 53BP1 binds to lamins A/C via its Tudor domain, and this is abrogated by DNA damage. Lamins A/C regulate 53BP1 levels and consequently lamin A/C-null HDF display a 53BP1 null-like phenotype. Our data favour a model in which lamins A/C maintain a nucleoplasmic pool of 53BP1 in order to facilitate its rapid recruitment to sites of DNA damage and could explain why an absence of lamin A/C accelerates aging.

Endothelial nuclear lamina is not required for glucocorticoid receptor nuclear import but does affect receptor-mediated transcription activation

The lamina serves to maintain the nuclear structure and stiffness while acting as a scaffold for heterochromatin and many transcriptional proteins. Its role in endothelial mechanotransduction, specifically how nuclear mechanics impact gene regulation under shear stress, is not fully understood. In this study, we successfully silenced lamin A/C in bovine aortic endothelial cells to determine its role in both glucocorticoid receptor (GR) nuclear translocation and glucocorticoid response element (GRE) transcriptional activation in response to dexamethasone and shear stress. Nuclear translocation of GR, an anti-inflammatory nuclear receptor, in response to dexamethasone or shear stress (5, 10, and 25 dyn/cm(2)) was observed via time-lapse cell imaging and quantified using a Bayesian image analysis algorithm. Transcriptional activity of the GRE promoter was assessed using a dual-luciferase reporter plasmid. We found no dependence on nuclear lamina for GR translocation from the cytoplasm into the nucleus. However, the absence of lamin A/C led to significantly increased expression of luciferase under dexamethasone and shear stress induction as well as changes in histone protein function. PCR results for NF-κB inhibitor alpha (NF-κBIA) and dual specificity phosphatase 1 (DUSP1) genes further supported our luciferase data with increased expression in the absence of lamin. Our results suggest that absence of lamin A/C does not hinder passage of GR into the nucleus, but nuclear lamina is important to properly regulate GRE transcription. Nuclear lamina, rather than histone deacetylase (HDAC), is a more significant mediator of shear stress-induced transcriptional activity, while dexamethasone-initiated transcription is more HDAC dependent. Our findings provide more insights into the molecular pathways involved in nuclear mechanotransduction.

Lamin A/C is Expressed in Pluripotent Mouse Embryonic Stem Cells

The pluripotent nature of embryonic stem cells (ESC) is associated with a dynamic open chromatin state and an irregular nuclear shape. It has been postulated that the absence of Lamin A/C contributes to these features. However, we show that mouse ESCs express low, yet readily detectable, amounts of Lamin A/C at both the RNA and protein levels. Full-length transcripts of both isoforms were readily detected by q-PCR and deep RNA sequencing. Additionally, protein expression was validated in multiple primary and established ESC lines by immunoblotting using several independent antibodies. Immunofluorescence labeling showed localization of Lamin A/C at the nuclear periphery of all Oct4/Nanog double-positive ESC lines examined, as well as in the inner cell mass of blastocysts. Our results demonstrate ESCs do express low levels of Lamin A/C, thus models linking pluripotency and nuclear dynamics with the absence of Lamin A/C need to be revisited.

Conserved cysteine residues in the mammalian lamin A tail are essential for cellular responses to ROS generation

Pre-lamin A and progerin have been implicated in normal aging, and the pathogenesis of age-related degenerative diseases is termed 'laminopathies'. Here, we show that mature lamin A has an essential role in cellular fitness and that oxidative damage to lamin A is involved in cellular senescence. Primary human dermal fibroblasts (HDFs) aged replicatively or by pro-oxidants acquire a range of dysmorphic nuclear shapes. We observed that conserved cysteine residues in the lamin A tail domain become hyperoxidized in senescent fibroblasts, which inhibits the formation of lamin A inter- and intramolecular disulfide bonds. Both in the absence of lamin A and in the presence of a lamin A cysteine-to-alanine mutant, which eliminates these cysteine residues (522, 588, and 591), mild oxidative stress induced nuclear disorganization and led to premature senescence as a result of decreased tolerance to ROS stimulators. Human dermal fibroblasts lacking lamin A or expressing the lamin A cysteine-to-alanine mutant displayed a gene expression profile of ROS-responsive genes characteristic of chronic ROS stimulation. Our findings suggest that the conserved C-terminal cysteine residues are essential for lamin A function and that loss or oxidative damage to these cysteine residues promotes cellular senescence.

Decreased Bone Formation and Osteopenia in Lamin A/C-Deficient Mice

Age-related bone loss is associated with changes in bone cellularity with characteristically low levels of osteoblastogenesis. The mechanisms that explain these changes remain unclear. Although recent in vitro evidence has suggested a new role for proteins of the nuclear envelope in osteoblastogenesis, the role of these proteins in bone cells differentiation and bone metabolism in vivo remains unknown. In this study, we used the lamin A/C null (Lmna −/−) mice to identify the role of lamin A/C in bone turnover and bone structure in vivo. At three weeks of age, histological and micro computed tomography measurements of femurs in Lmna −/− mice revealed a significant decrease in bone mass and microarchitecture in Lmna −/− mice as compared with their wild type littermates. Furthermore, quantification of cell numbers after normalization with bone surface revealed a significant reduction in osteoblast and osteocyte numbers in Lmna −/− mice compared with their WT littermates. In addition, Lmna −/− mice have significantly lower osteoclast number, which show aberrant changes in their shape and size. Finally, mechanistic analysis demonstrated that absence of lamin A/C is associated with increase expression of MAN-1 a protein of the nuclear envelope closely regulated by lamin A/C, which also colocalizes with Runx2 thus affecting its capacity as osteogenic transcription factor. In summary, these data clearly indicate that the presence of lamin A/C is necessary for normal bone turnover in vivo and that absence of lamin A/C induces low bone turnover osteopenia resembling the cellular changes of age-related bone loss.

Specific contribution of lamin A and lamin C in the development of laminopathies

Mutations in the lamin A/C gene are involved in multiple human disorders for which the pathophysiological mechanisms are partially understood. Conflicting results prevail regarding the organization of lamin A and C mutants within the nuclear envelope (NE) and on the interactions of each lamin to its counterpart. We over-expressed various lamin A and C mutants both independently and together in COS7 cells. When expressed alone, lamin A with cardiac/muscular disorder mutations forms abnormal aggregates inside the NE and not inside the nucleoplasm. Conversely, the equivalent lamin C organizes as intranucleoplasmic aggregates that never connect to the NE as opposed to wild type lamin C. Interestingly, the lamin C molecules present within these aggregates exhibit an abnormal increased mobility. When co-expressed, the complex formed by lamin A/C aggregates in the NE. Lamin A and C mutants for lipodystrophy behave similarly to the wild type. These findings reveal that lamins A and C may be differentially affected depending on the mutation. This results in multiple possible physiological consequences which likely contribute in the phenotypic variability of laminopathies. The inability of lamin C mutants to join the nuclear rim in the absence of lamin A is a potential pathophysiological mechanism for laminopathies.

Evidence that Proteasome-Dependent Degradation of the Retinoblastoma Protein in Cells Lacking A-Type Lamins Occurs Independently of Gankyrin and MDM2

BackgroundA-type lamins, predominantly lamins A and C, are nuclear intermediate filaments believed to act as scaffolds for assembly of transcription factors. Lamin A/C is necessary for the retinoblastoma protein (pRB) stabilization through unknown mechanism(s). Two oncoproteins, gankyrin and MDM2, are known to promote pRB degradation in other contexts. Consequently, we tested the hypothesis that gankyrin and/or MDM2 are required for enhanced pRB degradation in Lmna−/− fibroblasts. Principal Findings. To determine if gankyrin promotes pRB destabilization in the absence of lamin A/C, we first analyzed its protein levels in Lmna−/− fibroblasts. Both gankyrin mRNA levels and protein levels are increased in these cells, leading us to further investigate its role in pRB degradation. Consistent with prior reports, overexpression of gankyrin in Lmna +/+ cells destabilizes pRB. This decrease is functionally significant, since gankyrin overexpressing cells are resistant to p16ink4a-mediated cell cycle arrest. These findings suggest that lamin A-mediated degradation of pRB would be gankyrin-dependent. However, effective RNAi-enforced reduction of gankyrin expression in Lmna−/− cells was insufficient to restore pRB stability. To test the importance of MDM2, we disrupted the MDM2-pRB interaction by transfecting Lmna−/− cells with p14arf. p14arf expression was also insufficient to stabilize pRB or confer cell cycle arrest, suggesting that MDM2 also does not mediate pRB degradation in Lmna−/− cells.Conclusions/SignificanceOur findings suggest that pRB degradation in Lmna−/− cells occurs by gankyrin and MDM2-independent mechanisms, leading us to propose the existence of a third proteasome-dependent pathway for pRB degradation. Two findings from this study also increase the likelihood that lamin A/C functions as a tumor suppressor. First, protein levels of the oncoprotein gankyrin are elevated in Lmna−/− fibroblasts. Second, Lmna−/− cells are refractory to p14arf-mediated cell cycle arrest, as was previously shown with p16ink4a. Potential roles of lamin A/C in the suppression of tumorigenesis are discussed.

Change of bottom water conditions at intermediate depths of the Oyashio region, NW Pacific over the past 20,000 yrs

The North Pacific Intermediate Water (NPIW), source water (Oyashio Intermediate Water; OYIW) of which originates east of the southern Kuril Islands, plays an important role in the carbon cycle of the Pacific Ocean. The spatio-temporal changes of NPIW, however, have yet to be clarified. Because of OYIW flowing in the Oyashio region, from east of the southern Kuril Islands through south of Hokkaido to east of Honshu, it is important to understand past bottom water changes at intermediate depths of this region for study of the past NPIW. Two sediment cores, GH02-1030 and MD01-2409, were collected from south of eastern and central Hokkaido. Lithology and physical properties of the cores recorded well the surface and bottom water conditions. Higher diatom productivity in the surface waters led to diatomaceous sediments with higher water contents and lower grain densities during the last deglaciation and late Holocene. These lithological changes occurred not only at the two studied cores but also at several other sites along the western margin of the NW Pacific. Benthic foraminiferal assemblages and occurrence of parallel lamination indicated such a dysoxic bottom water condition during the last deglaciation. Absence of lamination in the late Holocene horizon suggested a somewhat higher dissolved oxygen concentration in bottom water than that during the last deglaciation. On the basis of benthic foraminifer assemblages corresponding to strengthening of intermediate water circulation inferred from coarsening of sediment grain size and decreasing of sedimentation rate indicating stronger winnowing effects, it appears that the bottom water oxygen level increased during the Younger Dryas cold period.

Formation of nuclear splicing factor compartments is independent of lamins A/C.

Nuclear lamins are major architectural elements of the mammalian cell nucleus, and they have been implicated in the functional organization of the nuclear interior, possibly by providing structural support for nuclear compartments. Colocalization studies have suggested a structural role for lamins in the formation and maintenance of pre-mRNA splicing factor compartments. Here, we have directly tested this hypothesis by analysis of embryonic fibroblasts from knock-out mice lacking A- and C-type lamins. We show that the morphology and cellular properties of splicing factor compartments are independent of A- and C-type lamins. Genetic loss of lamins A/C has no effect on the cellular distribution of several pre-mRNA splicing factors and does not affect the compartment morphology as examined by light and electron microscopy. The association of splicing factors with the nuclear matrix fraction persists in the absence of lamins A/C. Live cell microscopy demonstrates that the intranuclear positional stability of splicing factor compartments is maintained and that the exchange dynamics of SF2/ASF between the compartments and the nucleoplasm is not affected by loss of lamin A/C. Our results demonstrate that formation and maintenance of intranuclear splicing factor compartments is independent of lamins A/C, and they argue against an essential structural role of lamins A/C in splicing factor compartment morphology.

On the evolution of the oxygen minimum zone in the Arabian Sea during Holocene time and its relation to the South Asian monsoon

Abstract The evolution of the oxygen minimum zone within the permanent thermocline of the Arabian Sea (AS) during early and mid-Holocene time was reconstructed from a laminated sediment core taken from the Pakistani continental margin (316 m water depth). A trace metal proxy for water column ventilation (authigenic U) was extracted by principal component analysis from a large dataset of inorganic and total organic carbon (TOC) measurements. This proxy is compared with preservation of lamination and paired benthic-planktonic 14 C data. The latter record the Δ 14 C depth gradient in the AS and may provide a sensitive indicator for ventilation by enhanced surface convection. Laminated sediments were preserved between 10 and 7.5 ka bp on the Pakistani continental margin and accumulated authigenic U independently from TOC accumulation. The inferred reducing conditions in the AS thermoline are in agreement with high palaeoproductivity in the western AS upwelling region. Century-scale variability in northern AS surface hydrography (recorded as δ 18 O in planktonic foraminifera) is reflected in the accumulation of authigenic U on the Pakistani margin. The agreement of AS surface conditions, which generally reflect the South Asian monsoon (SAM), with ventilation of the OMZ confirms a dominant influence of the SAM and summer monsoon upwelling in particular on AS thermocline ventilation during early Holocene time. However, the preservation of laminated sediments off Pakistan and palaeoproductivity in the western AS disagree before 10 ka cal. bp, and between 7.5 and 5.5 cal. ka bp. Here, the absence of lamination indicates better ventilation of the thermocline, whereas palaeoproductivity in the upwelling region was high. This suggests that other factors may also have contributed in variable proportions to AS thermocline ventilation. At present, these factors include lateral advection of oxygenated Central Indian Water and ventilation by winter surface convection in the northern AS.

Purification of intact nuclear lamina and identification of novel laminlike proteins in Raji, a cell line devoid of lamins A and C

Research on the structure of the nuclear lamina and the nuclear matrix of cells devoid of lamins A and C has been hampered by the fact that intact residual nuclear structures are difficult to isolate from such cells. In this paper, we show that some extraction parameters, such as buffer composition and the nature of the detergent used to remove nuclear membranes, are critical for achieving isolation of whole nuclear residual structures from the lymphoblastic cell line Raji, used as a model for cells without lamins A and C. Electron microscopic analysis shows that the nuclear lamina of Raji cells is formed by a network of intermediate-size filaments interrupted with circular discontinuities. Both lamins B1 and B2, and lamin D/E, are present in this structure. In addition, a group of 45-kDa proteins or intermediate filament protein--reacting proteins (IFA-RPs), located uniquely in the lamina, were found to exhibit the same immunological and chemical characteristics as lamins. Although they behave like nuclear lamins, microsequencing analysis of the IFA-RPs has revealed no homology with known lamins. These IFA-RPs may contribute to the formation of the nuclear lamina filament network in the absence of lamins A and C.

A geological approach toward developing a mudrock-durability classification system

Relationships between durability and lithologic characteristics of 61 mudrock samples from North America were investigated with the objective of developing a mudrock-durability classification based on lithologic characteristics. Second-cycle slake-durability index (Id2) was used as a measure of durability, whereas clay content, clay-mineral composition, texture, microfracture frequency, absorption, adsorption, dry density, void ratio, and Atterberg limits were used to characterize mudrock lithology. Based upon the amount of clay-size material, the presence or absence of laminations, and the degree of induration, the mudrocks were subdivided into claystones, mudstones, siltstones, shales, and argillites. The relationships between durability and lithologic characteristics were investigated separately for each class of mudrocks. The results show that different lithologic characteristics best correlate with the durability of each class of mudrocks. The durability of claystones correlates best with the amount of expandable clay minerals and that of mudstones with the frequency of microfractures. The degree of consolidation, as expressed by absorption, influences the durability of both siltstones and shales. The durability of argillites is related to their crystalline texture. Lithologic characteristics can be quantitatively related to a durability classification proposed herein that recognizes three classes of durability: low (Id2 < 50%), medium (Id2 = 50%–85%), and high (Id2 > 85%). Key words : mudrock, durability, lithologic characteristics, classification.

Facies Implications of Trichichnus and Chondrites in Turbidites and Hemipelagites, Marnoso-Arenacea Formation (Miocene), Northern Apennines, Italy

Trichichnus, a thread-like burrow possibly the work of sipunculan worms, is widespread in Bouma E (turbidite claystone) and H (hemipelagic claystone) layers and some thin turbidite sandstone beds in basin-plain and outer fan-lobe deposits of the Marnoso-arenacea Formation. Trichichnus closely resembles that described elsewhere in chalk and marlstone, although the burrows are smaller (mean diameter=0.13 mm) and burrow curvature is tighter. Trichichnus fills are darker than the host claystone because of high organic content and disseminated pyrite. Any distinctive internal structure of the burrow wall or fill was destroyed by pyrite growth. Trichichnus is most abundant in Bouma E layers, where burrow spacing ranges from 0.4 to 50 cm and burrows extend to depths of 160 cm. The Trichichnus maker commonly burrowed vertically down through E and D layers (clay and silt) and then horizontally on top of C layers (sand). The burrows also vertically penetrate Bouma C sandstone layers up to 6 cm thick, but they are rare in beds thicker than 3 cm. They are less abundant or not well displayed in H layers where Chondrites predominates. Trichichnus overprints Chondrites. Following deposition of the Contessa megaturbidite, which exceeds 9 m in thickness, the sediment surface was repopulated chieflymore » by Trichichnus and Chondrites producers. Trichichnus extends 160 cm below the top of the Contessa, whereas Chondrites extend only to 64 cm. This suggests a greater tolerance of Trichichnus makers to low in situ oxygen levels. The near absence of laminations in the E division of the Contessa megabed may be the result of Trichichnus burrows that were not pyritized and which lack textural identity.« less