I didn't know there were distinct differences between gram-positive and gram-negative bacteria when it came to quorum sensing, but it seems as though there is:
In gram negative bacteria, acyl-homoserine lactone type molecules serve as the main signalling molecules while lipid, peptide, and amino acid based signalling molecules infrequently serve as signalling molecules. Furthermore, in gram-negative bacteria, there is one well conserved mechanism for controlling quorum response. Gram-positive bacteria, on the other hand, use peptides or modified peptides as the primary means of signaling; and also differing from gram-negative bacteria, there are several different mechanisms found within the class which are used to gain quorum responses.
In G+ bacteria, the two main quorum sensing mechanisms are apparently as follows:
Two-component signal transduction, in which the peptide signal works by binding to a sensor protein, histidine kinase, located in the cell membrane of the bacterium. The activation of the histidine kinase leads to phosphorylation of response-regulating protein, and interaction with another regulatory protein facilitates transcriptional activation.
Internalization, in which the signal molecules are transported into the responder cell to interact with intracellular effectors.
G- bacteria on the other hand, synthesize autoinducers, effector molecules that can diffuse freely through the cell membrane and trigger cell response when a certain concentration threshold is reached. I do not know how or if these differences are related to cell wall structure.
When it comes to endospore formation, all I know of the difference between the two is that this is by far most common in gram-positive bacteria.