BackgroundMost bacteria are grown in a binary fission way meaning a bacterial cell is equally divided into two. Polyhydroxyalkanoates (PHA) can be accumulated as inclusion bodies by bacteria. The cell division way and morphology have been shown to play an important role in regulating the bacterial growth and PHA storages.ResultsThe common growth pattern of Escherichia coli was changed to multiple fission patterns by deleting fission related genes minC and minD together, allowing the formation of multiple fission rings (Z-rings) in several positions of an elongated cell, thus a bacterial cell was observed to be divided into more than two daughter cells at same time. To further improve cell growth and PHA production, some genes related with division process including ftsQ, ftsL, ftsW, ftsN and ftsZ, together with the cell shape control gene mreB, were all overexpressed in E. coli JM109 ∆minCD. The changing pattern of E. coli cell growth and morphology resulted in more cell dry weights (CDW) and more than 80 % polyhydroxybutyrate (PHB) accumulation increases compared to its binary fission control grown under the same conditions.ConclusionsThis study clearly demonstrated that combined over-expression genes ftsQ, ftsW, ftsN, ftsL and ftsZ together with shape control gene mreB in multiple division bacterial E. coli JM109 ∆minCD benefited PHA accumulation. Our study provides useful information on increasing the yield of PHA by changing the cell division pattern and cell morphology of E. coli.Electronic supplementary materialThe online version of this article (doi:10.1186/s12934-016-0531-6) contains supplementary material, which is available to authorized users.

Background: DNA damage-induced activation of the Rac1/JNK cascade is required for apoptosis. Results: Upon chemotherapeutic drug treatment, Tiam1, a Rac1-specific GEF, is accumulated through inhibition of CK1/ ␤-TrCP-mediated degradation. Conclusion: DNA damage induces up-regulation of Tiam1, which contributes to Rac1/JNK activation. Significance: This work uncovers how the Rac1/JNK cascade is activated upon DNA damage signaling and subsequent apoptosis.