Carbonate minerals such as dolomite, kutnahorite or rhodochrosite are frequently, but not exclusively generated by microbial processes. In recent anoxic sediments, Mn(II)carbonate minerals (e.g. rhodochrosite, kutnahorite) derive mainly from the reduction of Mn(IV) compounds by anaerobic respiration. The formation of huge manganese-rich (carbonate) deposits requires effective manganese redox cycling in an oxygenated atmosphere. However, putative anaerobic pathways such as microbial nitrate-dependent manganese oxidation, anoxygenic photosynthesis and oxidation in ultraviolet light may facilitate manganese cycling even in an early Archean environment, without the availability of oxygen. In addition, manganese carbonates precipitate by microbially induced processes without change of the oxidation state, e.g. by pH shift. Hence, there are several ways how these minerals could have been formed biogenically and deposited in Precambrian sediments. We will summarize microbially induced manganese carbonate deposition in the presence and absence of atmospheric oxygen and we will make some considerations about the biogenic deposition of manganese carbonates in early Archean settings.

Pus1-dependent pseudouridylation occurs in many tRNAs and at multiple positions, yet the functional impact of this modification is incompletely understood. We analyzed the consequences of PUS1 deletion on the essential decoding of CAG (Gln) codons by tRNA^GlnCUG in yeast. Synthetic lethality was observed upon combining the modification defect with destabilized variants of tRNA^GlnCUG, pointing to a severe CAG-decoding defect of the hypomodified tRNA. In addition, we demonstrated that misreading of UAG stop codons by a tRNA^GlnCUG variant is positively affected by Pus1. Genetic approaches further indicated that mildly elevated temperature decreases the decoding efficiency of CAG and UAG via destabilized tRNA^GlnCAG variants. We also determined the misreading of CGC (Arg) codons by tRNA^HisGUG, where the CGC decoder tRNA^ArgICG contains Pus1-dependent pseudouridine, but not the mistranslating tRNA^His. We found that the absence of Pus1 increased CGC misreading by tRNA^His, demonstrating a positive role of the modification in the competition against non-synonymous near-cognate tRNA. Part of the in vivo decoding defects and phenotypes in pus1 mutants and strains carrying destabilized tRNA^GlnCAG were suppressible by additional deletion of the rapid tRNA decay (RTD)-relevant MET22, suggesting the involvement of RTD-mediated tRNA destabilization.

Yeast phenotypes associated with the lack of wobble uridine (U₃₄) modifications in tRNA were shown to be modulated by an allelic variation of SSD1, a gene encoding an mRNA-binding protein. We demonstrate that phenotypes caused by the loss of Deg1-dependent tRNA pseudouridylation are similarly affected by SSD1 allelic status. Temperature sensitivity and protein aggregation are elevated in deg1 mutants and further increased in the presence of the ssd1-d allele, which encodes a truncated form of Ssd1. In addition, chronological lifespan is reduced in a deg1 ssd1-d mutant, and the negative genetic interactions of the U₃₄ modifier genes ELP3 and URM1 with DEG1 are aggravated by ssd1-d. A loss of function mutation in SSD1, ELP3, and DEG1 induces pleiotropic and overlapping phenotypes, including sensitivity against target of rapamycin (TOR) inhibitor drug and cell wall stress by calcofluor white. Additivity in ssd1 deg1 double mutant phenotypes suggests independent roles of Ssd1 and tRNA modifications in TOR signaling and cell wall integrity. However, other tRNA modification defects cause growth and drug sensitivity phenotypes, which are not further intensified in tandem with ssd1-d. Thus, we observed a modification-specific rather than general effect of SSD1 status on phenotypic variation in tRNA modification mutants. Our results highlight how the cellular consequences of tRNA modification loss can be influenced by protein targeting specific mRNAs.

Clostridium litoraleis a Gram-positive, rod-shaped, and spore-forming bacterium, which is able to use amino acids such as glycine, sarcosine, proline, and betaine as single carbon and energy sources via Stickland reactions. The genome consists of a circular chromosome (3.41 Mb) and a circular plasmid (27 kb).