Mycobacterium tuberculosis and its clever approaches to escape the deadly macrophage.

Mycobacterium tuberculosis (Mt.b), a deadly disease causer, is a facultative parasite. This microorganism has developed several methods to defend itself, once internalized within specialised vacuoles in the macrophages. A wide array of receptors like the complement receptor mannose receptors, scavenger receptor assists the entry of the microbe within the phagocytic macrophages. However, Mt.b is clever enough to protect itself from the hostile environment of the macrophage thereby prevailing within it. The microbe can efficiently inhibit processes like phagosome-lysosome fusion, acidification of phagosomes, release of proinflammatory cytokines and stop crucial events like apoptosis. Additionally, it also adopts resistance to killing by reactive oxygen intermediates and reactive nitrogen intermediates. There are multiple genes both in host and the pathogen which are involved in this successful survival of Mt.b. The regulation of phagolysosome fusion is mediated by proteins such as Coronin, TlyA, SapM, PnkG, EsxH. The microbe has certain mechanisms to even acquire iron from the host cell, to withstand iron deprivation as a mode of host's defence mechanism. This review focuses on the various defensive adaptations acquired by Mt.b for fighting against the deprived conditions existing within the macrophages and their capability of proliferating successfully within it, thereby resulting in a diseased condition.

Complete Genome Sequences of the Novel Cluster BP Phages Infecting Streptomyces sanglieri, AxeJC, Cumberbatch, Eastland, Eklok, HFrancette, Ignacio, Piccadilly, and Vondra.

The Streptomyces sanglieri bacteriophages AxeJC, Cumberbatch, Eastland, Eklok, HFrancette, Ignacio, Piccadilly, and Vondra form a novel actinobacteriophage cluster, BP. These siphoviruses have circularly permuted genomes with an average size of 37,700 bp and a GC content of 71%. Each genome contains approximately 58 protein-coding genes, with no tRNAs.

Optimized Tools and Methods for Methanotroph Genome Editing.

Microbes with the capacity to use methane (CH4) as a carbon source (methanotrophs) have significant potential for the bioconversion of CH4-containing natural gas and anaerobic digestion-derived biogas to high value products. These organisms also play a vital role in the biogeochemical cycling of atmospheric CH4 by serving as the only known biological sink of this gas in terrestrial and aquatic ecosystems. Much is known regarding the enzymes and central metabolic pathways mediating CH4 utilization in these bacteria. However, large fundamental knowledge gaps exist regarding methanotroph physiology and responses to environmental stimuli, primarily due to a lack of efficient molecular tools to probe gene-function relationships. In this chapter, we describe several recently developed genetic tools and optimized genome editing methods that can be used for methanotroph metabolic engineering and to probe metabolic and physiological governing mechanisms in these unique bacteria.