Tit Bits

 

    Peroxisomes identified as 'fighters' in the battle against bacterial infections

 

    A new addition to the fight against bacteria comes in the unlikely form of an organelle that previously had no link to the immune response. University of Alberta researchers have found that peroxisomes are required for the cells in the innate immune response against bacteria and fungi. The discovery was first made in fruit flies. Research Associate Francesca Di Cara, together with Richard Rachubinski, Professor and Chair of the Department of Cell Biology and Andrew Simmonds, Cell Biology Associate Professor, partnered to create fruit flies that could be used specifically for studying peroxisomal disorders, which are rare genetic diseases affecting humans.


    Di Cara found that peroxisomes are necessary for proper functioning of the innate immune system, the body's first line of defense against microorganisms. The innate immune system is an ancient system of immunity that identifies, captures and processes a pathogen and then presents it to the acquired immune system. The peroxisomes also communicate to other organs that there is an infection. The team discovered that when the organelle's basic function is altered, this communication is lost and the organism does not fight the bacteria.

    "Understanding how the body fights infection has an impact on human health," says Di Cara. "We have to understand who the fighters in the organism are before we can identify what's failing in the battle against bacterial infections.“

    Peroxisomes are chemical factories that process complex fat molecules into simple forms and modify reactive oxygen molecules, which together act to signal cells and tissues to respond appropriately for the changes in their environment. Along with their collaborator Nancy Braverman from McGill University, the researchers used a mouse model to confirm that what they observed in the flies also occurred in a mammalian system.

    "To find organelles like peroxisomes that had no link whatsoever to fighting bacterial infections was a critical discovery, it will help expand the roles of what this important organelle does in innate immunity against bacterial and fungi and its involvement in viral signaling and the lethal peroxisome genetic diseases," says Rachubinski. As the threat of bacterial infections continues to grow, this discovery can help move our understanding of immunity forward.

 

Source: www.sciencedaily.com

 

Pause to read the traffic sign: Regulation of DNA transcription in bacteria

 

     One of the central tenets of biology is that information flows from DNA to RNA in order to encode proteins, which function in the cell. Arguably just as critical as the genetic code is the timing of this information flow. By producing the right RNA and right proteins at the right time, a cell can effectively strategize its survival and success. One such regulatory element, the riboswitch, has excited interest as a potential target for antibiotics. After over 10 years of research, Scientists of Goethe University together with colleagues from other universities have put together the puzzle pieces of a riboswitch-based regulatory process in the bacterium Bacillus subtilis, presenting the most extensive model of the timing of riboswitch action to date.

 

      A riboswitch is a short piece of RNA that can fold into different structures, depending on whether or not a small messenger molecule is binds to it. In transcriptional riboswitches, these different structures signal the nearby RNA polymerase to continue producing RNA or to stop. In their recent publication in ELife, the Schwalbe group and their collaborators released molecular structures of the xpt-pbuX riboswitch in the off-position after synthesis and in the on-position upon binding by the small messenger molecule guanine. They also demonstrated that this switch to the on-position takes a certain amount of time. This sets a certain requirement on this regulatory process.

 

 

Source: www.Phys.org



ENVIS CENTRE Newsletter Vol.15, Issue 3, Jul - Sep 2017
 
 
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