I haven’t said it yet, but I’m at the EMBO meeting in Barcelona (Spain) at the moment. I’ll attend some exciting workshops and lectures, but – last but not least – I’ll present a poster at the session dedicated to Genomics and Computational Biology on Tuesday. The satellite session is finished now and the opening talks and lectures took place after 6 pm in the Auditorium of the Palau des Congressos. Some impressions below 🙂
The opening began with a short introduction from Maria Leptin, the EMBO director. She presented the main objectives of the meeting (second edition): broadening molecular biology scope by inviting young scientists from various domains of life sciences as well as industrials. Afterwards, nice presentation of the current developments of life sciences in Spain was given by Luis Serrano, who finished attracting our attention to skilful pickpockets wandering around in Barcelona 😉
Afterwards, Prof. Richard Losick from Harvard University gave the opening lecture. It was titled “Life and death of a bacterial community”. The main part of it was focused on Bacillus subtilis. For those who did not attend, here is a summary.
Bacteria gather and create a community: this is commonly known as a biofilm. First, a question to be adressed is: how is a biofilm formation switched on? Microscopy pictures show that cells grow and enter the division process, but they do not separate physically. Thus, the clones are shaped as a chain; given that there are numerous chains from this kind, what is obtained at one point is an ensemble of parallel chains kept together thanks to what is called a matrix.
Studies have identified 3 important regulatory proteins: I, Slr, R. The latter two ones are mutually antagonistic: the R protein inhibits slr expression and the Slr protein sequesters the R protein, creating the complexe Slr°R. Cell separation is governed by autolysins: those are turned OFF by the complexe Slr°R. Therefore, cells do not separate and the chaining appears.
This interaction between Slr and R is a case of a double-negative loop. It has 2 states: the Slr-low state where the R protein represses the expression of slr and the Slr-high state where the produced Slr and R proteins form the complexe inhibiting the autolysins. This is a case of a bi-stable switch.
But: eventually, the loop must switch to the Slr-low state so that cells can go back to planktonic existance. How is this achieved? The Slr protein is not stable: as nutrients are exhausted, Slr is not replenished.
Ok, we know what triggers cell separation and free cells existance in this case. But how do the cells escape from the matrix? Whatever factor should be intervening to somehow degrade the matrix. It was shown that this particular factor is a combination of particular D-amino acids.
What are the D-amino acids doing? They are known to be present in the peptidoglycan of bacterial Gram+ cells. Sometimes, special D-amino acids can be incorporated instead of regular D-amino acids: the special ones are those “breaking” the biofilm.
How are those D-amino acids produced? Particular enzymes, namely the racemases (encoded by racX and ylmE), take care of this production. It was demonstrated that racX is repressed by Slr. So, when, in early times of the biofilm formation, Slr is abundant, racX is OFF. Later on, when Slr gets degraded, racX is progressively transcribed: therefore, D-amino acids can be produced.
Finally, Prof. Losick mentionned some experiments which adressed the question whether D-amino acids incorporation in the cell wall might be a signal for biofilm disassembly. When assayed in B. subtilis and S. aureus, this question is answered “yes”.
Given that Gram- bacteria (such as Pseudomonas) are also responsible for biofilm formation, it is worth to search for mechanisms in this case. To be continued then!
See you tomorrow for insights from workshops and conferences I’ve visited 🙂
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