Dynein Heavy Chain, Encoded by Two Genes in Agaricomycetes, Is Required for Nuclear Migration in Schizophyllum commune.

The white-rot fungus Schizophyllum commune (Agaricomycetes) was used to study the cell biology of microtubular trafficking during mating interactions, when the two partners exchange nuclei, which are transported along microtubule tracks. For this transport activity, the motor protein dynein is required. In S. commune, the dynein heavy chain is encoded in two parts by two separate genes, dhc1 and dhc2. The N-terminal protein Dhc1 supplies the dimerization domain, while Dhc2 encodes the motor machinery and the microtubule binding domain. This split motor protein is unique to Basidiomycota, where three different sequence patterns suggest independent split events during evolution. To investigate the function of the dynein heavy chain, the gene dhc1 and the motor domain in dhc2 were deleted. Both resulting mutants were viable, but revealed phenotypes in hyphal growth morphology and mating behavior as well as in sexual development. Viability of strain Δdhc2 is due to the higher expression of kinesin-2 and kinesin-14, which was proven via RNA sequencing.

RT1.L: a family of MHC class Ib genes of the rat major histocompatibility complex with a distinct promoter structure.

RT1.L class I antigens have originally been identified in LEW rats by LEW.1LV3-anti-LEW.1LM1 antisera and have been classified as nonclassical. We report now that LEW.1LV3-anti-LEW.1LM1 antisera react with three different antigens, termed RT1.L1, RT1.L2, and RT1.L3. This was found by serological analysis of a panel of transfectants expressing different class I genes of strain LEW with a LEW.1LV3-anti-LEW.1LM1 antiserum and two monoclonal antibodies (mAbs HT20 and HT21) generated in the same strain combination. The antiserum reacted with all three antigens: the two mAbs with RT1.L1 and RT1.L2, respectively. Sequence analysis showed that the genes encoding RT1.L1, RT1.L2, and RT1.L3 cluster together in a phylogenetic analysis of rat and mouse alpha(1)-alpha(2) sequences and that they share an unusual MHC class I promoter in which Enhancer A and B, as well as the interferon response element (IRE), are missing. Exchange of the promoter in RT1.L2 against the classical RT1.A promoter resulted in high surface expression in appropriate transfectants, indicating that the deviant promoter is responsible for the weak surface expression of the RT1.L2 gene. The very similar promoter structures of RT1.L1 and RT1.L3 are likely to contribute also to the weak expression of these genes. As RT1.L3 maps closely to the deletion in the mutant haplotype lm1, the RT1.L family can be located in the class I region extending from Bat1 to Pou5f1. Different from other allogeneic mAbs detecting known class I molecules encoded by genes of the RT1.C/E region, HT20 and HT21 react with a wide panel of strains carrying different RT1 haplotypes. This suggests that nonclassical class I genes of the RT1.L family are present in most RT1 haplotypes.