Linking food web functioning and habitat diversity for an ecosystem based management: a Mediterranean lagoon case-study.

We propose a modelling approach relating the functioning of a transitional ecosystem with the spatial extension of its habitats. A test case is presented for the lagoon of Venice, discussing the results in the context of the application of current EU directives. The effects on food web functioning due to changes related to manageable and unmanageable drivers were investigated. The modelling procedure involved the use of steady-state food web models and network analysis, respectively applied to estimate the fluxes of energy associated with trophic interactions, and to compute indices of food web functioning. On the long term (hundred years) temporal scale, the model indicated that the expected loss of salt marshes will produce further changes at the system level, with a lagoon showing a decrease in the energy processing efficiency. On the short term scale, simulation results indicated that fishery management accompanied by seagrass restoration measures would produce a slight transition towards a more healthy system, with higher energy cycling, and maintaining a good balance between processing efficiency and resilience. Scenarios presented suggest that the effectiveness of short term management strategies can be better evaluated when contextualized in the long term trends of evolution of a system. We also remark the need for further studying the relationship between habitat diversity and indicators of food web functioning.

Temporal and spatial changes of macroalgae and phytoplankton in a Mediterranean coastal area: the Venice lagoon as a case study.

Since the late 1980s the lagoon of Venice, a shallow Mediterranean coastal area, has experienced strong environmental changes. Macroalgae, which were the predominant primary producers of the lagoon, reduced markedly, but neither phytoplankton nor seagrasses replaced them. Temporal and spatial changes in macroalgal standing crop (SC) and phytoplankton concentration were investigated between 1987 and 1998. Maps of macroalgal SC show a marked declining trend. Biomass in fresh weight decreased from: 558 ktonnes in 1987, to 85 ktonnes in 1993 and to 8.7 ktonnes in 1998. As a whole, the biomass in 1998 was only 1.6% of the biomass recorded in 1987. Similarly the macroalgal net (NPP) and gross (GPP) primary production decreased from ca. 1502 and 9721 ktonnes year(-1) to ca. 44 and 229 ktonnes year(-1), respectively. In the early 1990s the clam Tapes philippinarum Adams & Reeve and seagrasses, especially Zostera marina Linnaeus, colonised the bottoms free of macroalgae, but the development of intense clam-fishing activities prevented both phytoplankton blooms and seagrass spreading. Maps of chlorophyll a drawn according to data collected in parallel to macroalgal standing crop show unchanged concentrations. Macroalgae changes are enhanced by comparing annual trends in four areas of the central lagoon during 1989-1992 and 1998-1999. In those areas phytoplankton also decreased significantly. Marked changes of some environmental variables strongly associated with the primary production were recorded both during the lagoon mapping and in the areas studied on a yearly basis.

Physical interaction of Cdc28 with Cdc37 in Saccharomyces cerevisiae.

The Cdc37 protein in Saccharomyces cerevisiae is thought to be a kinase-targeting subunit of the chaperone Hsp90. In a genetic screen, four protein kinases were identified as interacting with Cdc37 - Cdc5, Cdc7, Cdc15 and Cak1. This result underlines the importance of Cdc37 for the folding of protein kinases. In addition, we showed that Ydj1, a yeast DnaJ homolog belonging to the Hsp40 family of chaperones, genetically interacts with Cdc37. No physical interaction has so far been detected between Cdc37 and Cdc28, although genetic interactions (synthetic lethality and mutation suppression), and biochemical studies have suggested that these two proteins functionally interact. We found that, when separately expressed, the N-terminal lobe of Cdc28 interacted strongly with the C-terminal moiety of Cdc37 in a two-hybrid system. This was not the case for the full-length Cdc28 protein. We present models to explain these results.

Disruption and functional analysis of six ORFs of chromosome IV: YDL103c (QRI1), YDL105w (QRI2), YDL112w (TRM3), YDL113c, YDL116w (NUP84) and YDL167c (NRP1).

We have disrupted six ORFs (YDL103c, YDL105w, YDL112w, YDL113c, YDL116w and YDL167c) located on the left arm of chromosome IV. Except for YDL112w, the short flanking homology strategy was used to construct disruption cassettes using the KanMX4 marker. For YDL112w, a disruption cassette including the LEU2 gene was made. YDL103c and YDL105w are essential genes for vegetative growth. Disruption of YDL112w, YDL113c and YDL167c does not result in any detectable phenotype with the tests we used, while disruption of YDL116w confers slow growth, cryosensitivity and thermosensitivity, and the disrupted diploid homozygotes for the disruption failed to sporulate.

Involvement of the yeast DNA polymerase delta in DNA repair in vivo.

The POL3 encoded catalytic subunit of DNA polymerase delta possesses a highly conserved C-terminal cysteine-rich domain in Saccharomyces cerevisiae. Mutations in some of its cysteine codons display a lethal phenotype, which demonstrates an essential function of this domain. The thermosensitive mutant pol3-13, in which a serine replaces a cysteine of this domain, exhibits a range of defects in DNA repair, such as hypersensitivity to different DNA-damaging agents and deficiency for induced mutagenesis and for recombination. These phenotypes are observed at 24 degrees, a temperature at which DNA replication is almost normal; this differentiates the functions of POL3 in DNA repair and DNA replication. Since spontaneous mutagenesis and spontaneous recombination are efficient in pol3-13, we propose that POL3 plays an important role in DNA repair after irradiation, particularly in the error-prone and recombinational pathways. Extragenic suppressors of pol3-13 are allelic to sdp5-1, previously identified as an extragenic suppressor of pol3-11. SDP5, which is identical to HYS2, encodes a protein homologous to the p50 subunit of bovine and human DNA polymerase delta. SDP5 is most probably the p55 subunit of Pol delta of S. cerevisiae and seems to be associated with the catalytic subunit for both DNA replication and DNA repair.

Rig2, a RING finger protein that interacts with the Kin28/Ccl1 CTD kinase in yeast.

Kin28/Cell, a cyclin-dependent kinase, is essential for the in vivo phosphorylation of the C-terminal domain of the largest subunit of RNA polymerase II in Saccharomyces cerevisiae. In a search for mutations co-lethal with a thermosensitive kin28 mutation, we have identified genes whose products interact functionally with Kin28. In the present work, we have studied a new complementation group of synthetic lethal mutations. The corresponding gene, RIG2, encodes a predicted RING finger protein. Rig2 is likely to be a homolog of MAT1 of higher eukaryotes which forms a ternary complex with MO15(cdk7) and cyclin H. Our genetic data suggest that Rig2 is a component of transcription factor TFIIH. Transcription activity in a rig2-ts mutant is impeded at restrictive temperature. However, none of the rig2-ts mutants obtained was UV sensitive, suggesting that Rig2 is dispensable for nucleotide excision repair.

The KIN28 gene is required both for RNA polymerase II mediated transcription and phosphorylation of the Rpb1p CTD.

Kin28p, associated with cyclin Ccl1p, is a putative cyclin-dependent kinase (CDK) of the p34cdc2 family in Saccharomyces cerevisiae. Search for mutations co-lethal (syn mutations) with a kin28 thermosensitive mutation (kin28-ts3) has uncovered genetic interactions between gene KIN28 and genes RAD3, SIN4, STI1 and CDC37. The genetic interaction between KIN28 and the CDC37 cell division cycle gene suggests that a connection exists between the activity of CDK-Kin28p and cell-cycle progression. Both RAD3 and SIN4 gene products are implicated in the RNA polymerase II transcription process. Here we show that RNA polymerase II transcription is drastically reduced in a kin28-ts mutant, at restrictive temperature. This impairment correlates with a markedly decreased phosphorylation of the C-terminal domain (CTD) of the largest subunit of RNA polymerase II (Rpb1p). Thus, the Kin28 gene product is required in vivo for RNA polymerase II phosphorylation and transcriptional activity as recently suggested by experiments using an in vitro reconstituted system.