Recent changes in shelf hydrography in the Siberian Arctic : potential for subsea permafrost instability

Summer hydrographic data (1920–2009) show a dramatic warming of the bottom water layer over the eastern Siberian shelf coastal zone (<10 m depth), since the mid-1980s, by 2.1°C. We attribute this warming to changes in the Arctic atmosphere. The enhanced summer cyclonicity results in warmer air temperatures and a reduction in ice extent, mainly through thermodynamic melting. This leads to a lengthening of the summer open-water season and to more solar heating of the water column. The permafrost modeling indicates, however, that a significant change in the permafrost depth lags behind the imposed changes in surface temperature, and after 25 years of summer seafloor warming (as observed from 1985 to 2009), the upper boundary of permafrost deepens only by ∼1 m. Thus, the observed increase in temperature does not lead to a destabilization of methane-bearing subsea permafrost or to an increase in methane emission. The CH4 supersaturation, recently reported from the eastern Siberian shelf, is believed to be the result of the degradation of subsea permafrost that is due to the long-lasting warming initiated by permafrost submergence about 8000 years ago rather than from those triggered by recent Arctic climate changes. A significant degradation of subsea permafrost is expected to be detectable at the beginning of the next millennium. Until that time, the simulated permafrost table shows a deepening down to ∼70 m below the seafloor that is considered to be important for the stability of the subsea permafrost and the permafrost-related gas hydrate stability zone

Vinculin gene is non-essential in Drosophila melanogaster

AbstractVinculin is thought to be an important cytoskeletal protein in the linkage between actin cytoskeleton and integrin transmembrane receptors. We identified Vinculin (Vinc) gene in the X chromosome of D. melanogaster. Drosophila vinculin is highly homologous in its N- and C-terminal domains both to mammalian and nematode vinculins, and contains internal repeats and proline-rich region typical for vinculins. The X chromosome rearrangement In(1LR)pn2a was found to disrupt Vinc so that the coding sequence is interrupted by the (AAGAG)n satellite DNA. Northern analysis revealed that the Vinc transcript is completely absent in the In(1LR)pn2a homozygous flies. Surprisingly, these Vinc flies are viable and fertile. This finding highlights plasticity and adaptive capacity of cellular cytoskeletal and anchorage system

The differences between Cis-and Trans-Gene inactivation caused by heterochromatin in Drosophila

Position-effect variegation (PEV) is the epigenetic disruption of gene expression near the de novo-formed euchromatin-heterochromatin border. Heterochromatic cis-inactivation may be accompanied by the trans-inactivation of genes on a normal homologous chromosome in trans-heterozygous combination with a PEV-inducing rearrangement. We characterize a new genetic system, inversion In(2)A4, demonstrating cis-acting PEV as well as trans-inactivation of the reporter transgenes on the homologous nonrearranged chromosome. The cis-effect of heterochromatin in the inversion results not only in repression but also in activation of genes, and it varies at different developmental stages. While cis-actions affect only a few juxtaposed genes, trans-inactivation is observed in a 500-kb region and demonstrates а nonuniform pattern of repression with intermingled regions where no transgene repression occurs. There is no repression around the histone gene cluster and in some other euchromatic sites. trans-Inactivation is accompanied by dragging of euchromatic regions into the heterochromatic compartment, but the histone gene cluster, located in the middle of the trans-inactivated region, was shown to be evicted from the heterochromatin. We demonstrate that trans-inactivation is followed by de novo HP1a accumulation in the affected transgene; trans-inactivation is specifically favored by the chromatin remodeler SAYP and prevented by Argonaute AGO2

Repeat-associated siRNAs cause chromatin silencing of retrotransposons in the Drosophila melanogaster germline

Silencing of genomic repeats, including transposable elements, in Drosophila melanogaster is mediated by repeat-associated short interfering RNAs (rasiRNAs) interacting with proteins of the Piwi subfamily. rasiRNA-based silencing is thought to be mechanistically distinct from both the RNA interference and microRNA pathways. We show that the amount of rasiRNAs of a wide range of retroelements is drastically reduced in ovaries and testes of flies carrying a mutation in the spn-E gene. To address the mechanism of rasiRNA-dependent silencing of retrotransposons, we monitored their chromatin state in ovaries and somatic tissues. This revealed that the spn-E mutation causes chromatin opening of retroelements in ovaries, resulting in an increase in histone H3 K4 dimethylation and a decrease in histone H3 K9 di/trimethylation. The strongest chromatin changes have been detected for telomeric HeT-A elements that correlates with the most dramatic increase of their transcript level, compared to other mobile elements. The spn-E mutation also causes depletion of HP1 content in the chromatin of transposable elements, especially along HeT-A arrays. We also show that mutations in the genes controlling the rasiRNA pathway cause no derepression of the same retrotransposons in somatic tissues. Our results provide evidence that germinal Piwi-associated short RNAs induce chromatin modifications of their targets

Trans-inactivation: Repression in a wrong place

Trans-inactivation is the repression of genes on a normal chromosome under the influence of a rearranged homologous chromosome demonstrating the position effect variegation (PEV). This phenomenon was studied in detail on the example of brownDominant allele causing the repression of wild-type brown gene on the opposite chromosome. We have investigated another trans-inactivation-inducing chromosome rearrangement, In(2)A4 inversion. In both cases, brownDominant and In(2)A4, the repression seems to be the result of dragging of the euchromatic region of the normal chromosome into the heterochromatic environment. It was found that cis-inactivation (classical PEV) and trans-inactivation show different patterns of distribution along the chromosome and respond differently to PEV modifying genes. It appears that the causative mechanism of trans-inactivation is de novo heterochromatin assembly on euchromatic sequences dragged into the heterochromatic nuclear compartment. Trans-inactivation turns out to be the result of a combination of heterochromatin-induced position effect and the somatic interphase chromosome pairing that is widespread in Diptera