Novel Variants in GDF9 Gene Affect Promoter Activity and Litter Size in Mongolia Sheep

Litter size is an economically important trait in sheep breeding. The objectives of this study were as follows: (1) to ascertain if any of the 19 known variants in the BMPRIB, BMP15, and GDF9 genes are present and associated with the litter size of Mongolia sheep; (2) to identify novel variants in GDF9 and perform association analysis; and (3) to validate the effects of these GDF9 promoter variants on the activity of the gene. The results of the 19 known variants showed that the FecBB affected the litter size of Mongolia sheep (p < 0.001). The association analysis results of novel variants showed that the g.46544883A>G (GenBank accession: NC_040256, the same below) in the 3’ untranslated region (3’ UTR), the c.1040T>C (Phe347Ser) in the exon 2, and the g.46547859C>T SNP in the promotor of GDF9 were significantly associated with litter size of Mongolia ewes (p < 0.01, p < 0.05, and p < 0.001, respectively). In addition, the GDF9 promoter activity analysis showed that the C allele at the −332 position (g.46547859C>T) could decrease luciferase activity compared with the T allele (p < 0.01). Our findings may facilitate effective marker-assisted selection to increase litter size in Mongolia sheep populations, as well as bring new insights into GDF9 expression.

The TetR-Type Transcriptional Repressor RolR from Corynebacterium glutamicum Regulates Resorcinol Catabolism by Binding to a Unique Operator,rolO

ABSTRACTTherol(designated forresorcinol) gene clusterrolRHMDis involved in resorcinol catabolism inCorynebacterium glutamicum, and RolR is the TetR-type regulator. In this study, we investigated how RolR regulated the transcription of therolgenes inC. glutamicum. The transcription start sites and promoters ofrolRandrolHMDwere identified. Quantitative reverse transcription-PCR and promoter activity analysis indicated that RolR negatively regulated the transcription ofrolHMDand of its own gene. Further, a 29-bp operatorrolOwas located at the intergenic region ofrolRandrolHMDand was identified as the sole binding site for RolR. It contained two overlapping inverted repeats and they were essential for RolR-binding. The binding of RolR torolOwas affected by resorcinol and hydroxyquinol, which are the starting compounds of resorcinol catabolic pathway. These two compounds were able to dissociate RolR-rolOcomplex, thus releasing RolR from the complex and derepressing the transcription ofrolgenes inC. glutamicum. It is proposed that the binding of RolR to its operatorrolOblocks the transcription ofrolHMDand of its own gene, thus negatively regulated resorcinol degradation inC. glutamicum.