The Impact of Diffusive Water Vapor Transport on Snow Profiles in Deep and Shallow Snow Covers and on Sea Ice

Water vapor transport has been highlighted as a critical process in Arctic snowpacks, shaping the snow cover structure in terms of density, thermal conductivity, and temperature profile among others. Here, we present an attempt to describe the thermally-induced vertical diffusion of water vapor in the snow cover and its effects of the snowpack structure using the SNOWPACK model. Convection, that may also constitute a significant part of vapor transport, is not addressed. Assuming saturated conditions at the upper boundary of the snowpack and as initial condition, the vapor flux between snow layers is expressed by a 1-dimensional transient diffusion equation, which is solved with a finite difference routine. The implications on the snowpack of this vertical diffusive flux, are analyzed using metrics such as the cumulative density change due to diffusive vapor transport, the degree of over- or undersaturation, the instantaneous snow density change rate, and the percentage of snow density change. We present results for four different regions sampling the space of natural snow cover variability: Alpine, Subarctic, Arctic, and Antarctic sea ice. The largest impact of diffusive water vapor transport is observed in snow on sea ice in the Weddell Sea and the shallow Arctic snowpack. The simulations show significant density reductions upon inclusion of diffusive water vapor transport: cumulative density changes from diffusive vapor transport can reach �62 and �66 kg m�3 for the bottom layer in the shallow Arctic snowpack and snow on sea ice, respectively. For comparison, in deeper snow covers, they rarely exceed �40 kg m�3. This leads to changes in density for shallow snowpacks at the soil-snow interface in the range of �5 to �21%. Mirroring the density decease at depth is a thicker deposition layer above it with increase in density around 7.5%. Similarly, for the sea ice, the density decreased at the sea ice-snow interface by �20%. We acknowledge that vapor transport by diffusion may in some snow covers�such as in thin tundra snow�be small compared to convective transport, which will have to be addressed in future work

Observations of snow cover processes on Antarctic sea ice from in-situ and model studies

The snow cover on Antarctic sea ice impacts the energy, mass, and momentum balance of the sea ice cover, which in turn strongly influences fluxes between ocean, sea ice, and atmosphere. Despite the fact that snow depth is qualified as an Essential Climate Variable, the knowledge of the snow cover distribution and properties is still mostly vague and no large-scale (e.g. Antarctic wide) snow depth data product is available. Snow on Antarctic sea ice is characterized through a high spatial and temporal variability, and shows a highly heterogeneous internal stratification. This poses a challenge to air or space borne snow depth retrieval algorithms. Similarly, sea ice models are not yet able to resolve snow processes with enough accuracy. Here we present measurements of snow depth and physical snow properties along drift trajectories of autonomous Snow Buoys, which were deployed during several Polarstern cruises in the Weddell Sea since 2014. Resulting time series of snow depth show an event driven snow accumulation even during austral summer, whereas melting and a significant decrease of snow depth is only observed along the marginal sea ice zone. Additional analysis with the 1D multi-layer thermodynamic snow model SNOWPACK provides insights into internal processes such as snow to ice development cover along the trajectories. For these studies, SNOWPACK, which was previously used for land-based snow, has been extended with a sea ice module and is forced with re-analysis data. Comparisons between model and in-situ measurements show the capability of the model to reproduce the prevalent snow stratigraphy

Drug-induced eRF1 degradation promotes readthrough and reveals a new branch of ribosome quality control.

Suppression of premature termination codons (PTCs) by translational readthrough is a promising strategy to treat a wide variety of severe genetic diseases caused by nonsense mutations. Here, we present two potent readthrough promoters-NVS1.1 and NVS2.1-that restore substantial levels of functional full-length CFTR and IDUA proteins in disease models for cystic fibrosis and Hurler syndrome, respectively. In contrast to other readthrough promoters that affect stop codon decoding, the NVS compounds stimulate PTC suppression by triggering rapid proteasomal degradation of the translation termination factor eRF1. Our results show that this occurs by trapping eRF1 in the terminating ribosome, causing ribosome stalls and subsequent ribosome collisions, and activating a branch of the ribosome-associated quality control network, which involves the translational stress sensor GCN1 and the catalytic activity of the E3 ubiquitin ligases RNF14 and RNF25

Heritability in the Efficiency of Nonsense-Mediated mRNA Decay in Humans

BACKGROUND: In eukaryotes mRNA transcripts of protein-coding genes in which an intron has been retained in the coding region normally result in premature stop codons and are therefore degraded through the nonsense-mediated mRNA decay (NMD) pathway. There is evidence in the form of selective pressure for in-frame stop codons in introns and a depletion of length three introns that this is an important and conserved quality-control mechanism. Yet recent reports have revealed that the efficiency of NMD varies across tissues and between individuals, with important clinical consequences. PRINCIPAL FINDINGS: Using previously published Affymetrix exon microarray data from cell lines genotyped as part of the International HapMap project, we investigated whether there are heritable, inter-individual differences in the abundance of intron-containing transcripts, potentially reflecting differences in the efficiency of NMD. We identified intronic probesets using EST data and report evidence of heritability in the extent of intron expression in 56 HapMap trios. We also used a genome-wide association approach to identify genetic markers associated with intron expression. Among the top candidates was a SNP in the DCP1A gene, which forms part of the decapping complex, involved in NMD. CONCLUSIONS: While we caution that some of the apparent inter-individual difference in intron expression may be attributable to different handling or treatments of cell lines, we hypothesize that there is significant polymorphism in the process of NMD, resulting in heritable differences in the abundance of intronic mRNA. Part of this phenotype is likely to be due to a polymorphism in a decapping enzyme on human chromosome 3

Rapid decay of unstable Leishmania mRNAs bearing a conserved retroposon signature 3′-UTR motif is initiated by a site-specific endonucleolytic cleavage without prior deadenylation

We have previously shown that the Leishmania genome possess two widespread families of extinct retroposons termed Short Interspersed DEgenerated Retroposons (SIDER1/2) that play a role in post-transcriptional regulation. Moreover, we have demonstrated that SIDER2 retroposons promote mRNA degradation. Here we provide new insights into the mechanism by which unstable Leishmania mRNAs harboring a SIDER2 retroposon in their 3′-untranslated region are degraded. We show that, unlike most eukaryotic transcripts, SIDER2-bearing mRNAs do not undergo poly(A) tail shortening prior to rapid turnover, but instead, they are targeted for degradation by a site-specific endonucleolytic cleavage. The main cleavage site was mapped in two randomly selected SIDER2-containing mRNAs in vivo between an AU dinucleotide at the 5′-end of the second 79-nt signature (signature II), which represents the most conserved sequence amongst SIDER2 retroposons. Deletion of signature II abolished endonucleolytic cleavage and deadenylation-independent decay and increased mRNA stability. Interestingly, we show that overexpression of SIDER2 anti-sense RNA can increase sense transcript abundance and stability, and that complementarity to the cleavage region is required for protecting SIDER2-containing transcripts from degradation. These results establish a new paradigm for how unstable mRNAs are degraded in Leishmania and could serve as the basis for a better understanding of mRNA decay pathways in general

The Bicoid Stability Factor Controls Polyadenylation and Expression of Specific Mitochondrial mRNAs in Drosophila melanogaster

The bicoid stability factor (BSF) of Drosophila melanogaster has been reported to be present in the cytoplasm, where it stabilizes the maternally contributed bicoid mRNA and binds mRNAs expressed from early zygotic genes. BSF may also have other roles, as it is ubiquitously expressed and essential for survival of adult flies. We have performed immunofluorescence and cell fractionation analyses and show here that BSF is mainly a mitochondrial protein. We studied two independent RNAi knockdown fly lines and report that reduced BSF protein levels lead to a severe respiratory deficiency and delayed development at the late larvae stage. Ubiquitous knockdown of BSF results in a severe reduction of the polyadenylation tail lengths of specific mitochondrial mRNAs, accompanied by an enrichment of unprocessed polycistronic RNA intermediates. Furthermore, we observed a significant reduction in mRNA steady state levels, despite increased de novo transcription. Surprisingly, mitochondrial de novo translation is increased and abnormal mitochondrial translation products are present in knockdown flies, suggesting that BSF also has a role in coordinating the mitochondrial translation in addition to its role in mRNA maturation and stability. We thus report a novel function of BSF in flies and demonstrate that it has an important intra-mitochondrial role, which is essential for maintaining mtDNA gene expression and oxidative phosphorylation

The role of deadenylation in the degradation of unstable mRNAs in trypanosomes

Removal of the poly(A) tail is the first step in the degradation of many eukaryotic mRNAs. In metazoans and yeast, the Ccr4/Caf1/Not complex has the predominant deadenylase activity, while the Pan2/Pan3 complex may trim poly(A) tails to the correct size, or initiate deadenylation. In trypanosomes, turnover of several constitutively-expressed or long-lived mRNAs is not affected by depletion of the 5′–3′ exoribonuclease XRNA, but is almost completely inhibited by depletion of the deadenylase CAF1. In contrast, two highly unstable mRNAs, encoding EP procyclin and a phosphoglycerate kinase, PGKB, accumulate when XRNA levels are reduced. We here show that degradation of EP mRNA was partially inhibited after CAF1 depletion. RNAi-targeting trypanosome PAN2 had a mild effect on global deadenylation, and on degradation of a few mRNAs including EP. By amplifying and sequencing degradation intermediates, we demonstrated that a reduction in XRNA had no effect on degradation of a stable mRNA encoding a ribosomal protein, but caused accumulation of EP mRNA fragments that had lost substantial portions of the 5′ and 3′ ends. The results support a model in which trypanosome mRNAs can be degraded by at least two different, partially independent, cytoplasmic degradation pathways attacking both ends of the mRNA