Streptomyces are filamentous bacteria living mostly in the soil and best known for their ability to produce specialised metabolites (e.g. antibiotics). They grow as tip-extending, branching hyphal filaments to form a multicellular mycelium. New branches are established by the formation of a new growth zone on the lateral cell wall. Proteins responsible for this process are organised in complexes called polarisomes, with DivIVA being the best described component. We have developed a genetic screen based on DivIVA overexpression to identify proteins potentially interacting with DivIVA in Streptomyces albus. Among the hits was the important morphogenic genes encoding PknB (Ser/Thr kinase). We confirmed that deletion of pknB rescues S. albus from the effects of overexpressing DivIVA. Next, we studied the impact of pknB deletion in Streptomyces. A mass spectrometry phosphoproteome analysis indicated that absence of PknB alters the phosphorylation state of CslA, a cellulose synthase-like protein, containing a transglycosylase domain. Our research demonstrated that a phosphoablative mutant of CslA impacts its activity in β-glucan synthesis, as it displays a similar hypersensitivity to lysozyme as a CslA deletion strain. This highlights one pathway through which PknB affects the stability of the cell wall structure and possibly explains its impact in rescuing the cell from a lethal overproduction of DivIVA. Our findings highlight the role of PknB in maintaining the cellular structure and integrity of the Streptomyces cell wall.