Photosynthetic microalgae can capture solar energy and convert it to bioenergy and biochemical products. In nature or industrial processes, microalgae live together with bacterial communities and may maintain symbiotic relationships. In general interactions, microalgae exude dissolved organic carbon that becomes available to bacteria. In return, the bacteria remineralize sulphur, nitrogen and phosphorous to support the further growth of microalgae. In specific interactions, heterotrophic bacteria supply B vitamins as organic cofactors or produce siderophores to bind iron, which could be utilized by microalgae, while the algae supply fixed carbon to the bacteria in return. In this review, we focus on mutualistic relationship between microalgae and bacteria, summarizing recent studies on the mechanisms involved in microalgae-bacteria symbiosis. Symbiotic bacteria on promoting microalgal growth are described and the relevance of microalgae-bacteria interactions for biofuel production processes is discussed. Symbiotic microalgae-bacteria consortia could be utilized to improve microalgal biomass production and to enrich the biomass with valuable chemical and energy compounds. The suitable control of such biological interactions between microalgae and bacteria will help to improve the microalgae-based biomass and biofuel production in the future.

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Chromosome V of the Saccharomyces carlsbergensis lager yeast strain 244, a yeast not amenable to tetrad analysis, was analysed genetically in S. cerevisiae genetic standard strains. This was achieved by crossing meiotic progeny of the lager yeast with S. cerevisiae strains carrying karl as well as the chromosome V markers canl, ura3, his1, ilvl, and rad3. From the transitory heterokaryons formed we selected strains retaining the characteristics of the recipient strain but having become prototrophic for uracil, histidine, and isoleucine. The resulting strains were disomic for chromosome V, having acquired a chromosome V from S. cadsbergensis in addition to the normal S. cerevisiae chromosome complement (chromosome addition strains). They were of two classes: In one class the transferred chromosome hardly recombines with the S. cerevisiae chromosome V in the region CAN1 -RAD3, which covers almost the entire known map. In the other class, the transferred chromosome recombined at normal levels. We conclude that S. carlsbergensis harbors two structurally different chromosomes V; one being homologous and one homoeologous to the S. cerevisiae chromosome. By use of the CAN1 locus, strains were selected which by mitotic chromosome loss had their normal chromosome V substituted by either the homologous or the homoeologous S. carlsbergensis chromosome, showing that these chromosomes are fully functional in S. cerevisiae. Tetrad analysis of the chromosome substitution strains confirmed the very different genetic behavior of the two S. carlsbergensis chromosomes V. In spite of the almost complete absence of recombination between the homoeologous chromosome and the S. cerevisiae chromosome, disjunction at meiosis appears normal, as indicated by high spore viability.Genomic Southern hybridizations with the probes CAN1, URA3, CYC7, and ILV1 could not detect any nucleotide sequence differences between these loci on the recombining S. carlsbergensis chromosome and the S. cerevisiae alleles. Under standard stringency (68 ~ 0.1 xSSC), hybridization of the probes to DNA from the strain with the homoeologous chromosome was only observed in the case oflLVl, where weak hybridization was found, indicating a considerable difference in nucleotide sequence.To further study the extent ofnucleotide sequence inhomology, the two different ILV1 genes ofS. carlsbergensis were cloned in ~ vectors. Mapping of 16 restriction enzyme sites showed identity between the allele located on the recombining chromosome and the ILV1 gene of S. cerevisiae. The nucleotide sequence of the ILV1 gene of the non-recombining chromosome was by restriction site mapping found to be very different from that of the S. cerevisiae allele.

The bap1 mutant of Saccharomyces cerevisiae was previously isolated by its reduced uptake of branched-chain amino acids. In the present study, the corresponding wild-type gene was cloned and partial sequencing and subsequent genetic analysis revealed identity to STP1, a gene involved in tRNA maturation. The decrease in amino-acid uptake caused by stp1 mutations is independent of GCN4. It was previously found that the BAP2 promoter can be activated by the presence of amino acids, notably leucine, in the medium. We found that this activation depends on STP1. As a simple hypothesis we propose that Stp1p is a transcription factor which activates BAP2, and probably other amino-acid permease genes.

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