Bandarupalli Venkata Vinay Kumar, St-Pierre Benoit
Department of Animal Science, South Dakota State University, Animal Science Complex, Box 2170, Brookings, SD 57007, USA.
GenMark Diagnostics, 5964 La Place Ct, Carlsbad, CA 92008, USA.
Microorganisms. 2023 Mar 4;11(3):658. doi: 10.3390/microorganisms11030658.
In ruminant livestock production, ruminal acidosis is an unintended consequence of the elevated dietary intake of starch-rich feedstuffs. The transition from a state of subacute acidosis (SARA) to acute acidosis is due in large part to the accumulation of lactate in the rumen, which is a consequence of the inability of lactate utilizers to compensate for the increased production of lactate. In this report, we present the 16S rRNA gene-based identification of two bacterial operational taxonomic units (OTUs), Bt-01708_Bf (89.0% identical to ) and Bt-01899_Ap (95.3% identical to ), that were enriched from rumen fluid cultures in which only lactate was provided as an exogenous substrate. Analyses of in-silico-predicted proteomes from metagenomics-assembled contigs assigned to these candidate ruminal bacterial species (Bt-01708_Bf: 1270 annotated coding sequences, 1365 hypothetical coding sequences; Bt-01899_Ap: 871 annotated coding sequences, 1343 hypothetical coding sequences) revealed genes encoding lactate dehydrogenase, a putative lactate transporter, as well as pathways for the production of short chain fatty acids (formate, acetate and butyrate) and for the synthesis of glycogen. In contrast to these shared functions, each OTU also exhibited distinct features, such as the potential for the utilization of a diversified set of small molecules as substrates (Bt-01708_Bf: malate, quinate, taurine and polyamines) or for the utilization of starch (Bt-01899_Ap: alpha-amylase enzymes). Together, these results will contribute to the continued characterization of ruminal bacterial species that can metabolize lactate into distinct subgroups based on other metabolic capabilities.
在反刍家畜生产中,瘤胃酸中毒是富含淀粉的饲料摄入增加带来的意外后果。从亚急性酸中毒(SARA)状态转变为急性酸中毒,很大程度上是由于瘤胃中乳酸的积累,这是乳酸利用菌无法补偿乳酸产量增加的结果。在本报告中,我们展示了基于16S rRNA基因对两个细菌操作分类单元(OTU)的鉴定,即Bt-01708_Bf(与 89.0%相同)和Bt-01899_Ap(与 95.3%相同),它们是从仅以乳酸作为外源底物的瘤胃液培养物中富集得到的。对分配给这些候选瘤胃细菌物种的宏基因组组装重叠群的计算机预测蛋白质组分析(Bt-01708_Bf:1270 个注释编码序列,1365 个假设编码序列;Bt-01899_Ap:871 个注释编码序列,1343 个假设编码序列)揭示了编码乳酸脱氢酶、一种假定的乳酸转运蛋白的基因,以及短链脂肪酸(甲酸、乙酸和丁酸)的产生途径和糖原合成途径。与这些共同功能相反,每个OTU还表现出不同的特征,例如利用多种小分子作为底物的潜力(Bt-01708_Bf:苹果酸、奎尼酸、牛磺酸和多胺)或利用淀粉的潜力(Bt-01899_Ap:α-淀粉酶)。这些结果共同将有助于继续表征能够根据其他代谢能力将乳酸代谢为不同亚组的瘤胃细菌物种。