Regulation of Drosophila mesoderm migration by phosphoinositides and the PH domain of the Rho GTP exchange factor Pebble.

The Drosophila RhoGEF Pebble (Pbl) is required for cytokinesis and migration of mesodermal cells. In a screen for genes that could suppress migration defects in pbl mutants we identified the phosphatidylinositol phosphate (PtdInsP) regulator pi5k59B. Genetic interaction tests with other PtdInsP regulators suggested that PtdIns(4,5)P2 levels are important for mesoderm migration when Pbl is depleted.

Snail-dependent repression of the RhoGEF pebble is required for gastrulation consistency in Drosophila melanogaster.

The Rho GTP exchange factor, Pebble (Pbl), long recognised as an essential activator of Rho during cytokinesis, also regulates mesoderm migration at gastrulation. Like other cell cycle components, pbl expression patterns broadly correlate with proliferative tissue. Surprisingly, in spite of its role in the early mesoderm, pbl is downregulated in the presumptive mesoderm before ventral furrow formation.

Polo kinase interacts with RacGAP50C and is required to localize the cytokinesis initiation complex.

The assembly and constriction of an actomyosin contractile ring in cytokinesis is dependent on the activation of Rho at the equatorial cortex by a complex, here termed the cytokinesis initiation complex, between a microtubule-associated kinesin-like protein (KLP), a member of the RacGAP family, and the RhoGEF Pebble. Recently, the activity of the mammalian Polo kinase ortholog Plk1 has been implicated in the formation of this complex. We show here that Polo kinase interacts directly with the cytokinesis initiation complex by binding RacGAP50C.

The effect of methyl glyoxal on cell division and the synthesis of protein and DNA in synchronous and asynchronous cultures of Escherichia coli B/r.

Methyl glyoxal inhibits the growth of Escherichia coli in synchronous and asynchronous culture. The inhibition of growth is accompanied by immediate inhibition of protein synthesis and of the initiation of replication of DNA. When methyl glyoxal is added after initiation of a round of replication the elongation of new DNA chains is not inhibited.

Excision repair of cis-diamminedichloroplatinum(II)-induced damage to DNA of Chinese hamster cells.

Platinum was lost from the DNA of cis-diamminedichloroplatinum(II) [cis-Pt(II)]-treated exponentially growing Chinese hamster V79-379A cells with a half-life of 28 hr. By contrast, platinum was lost from the DNA of cells treated in stationary-phase culture with a half-life of 4 days. Cells treated in and allowed to remain as a stationary-phase culture maintained an intact and apparently viable appearance.

Effects of cis-platinum(II) diamminedichloride on survival and the rate of DNA synthesis in synchronously growing Chinese hamster V79-379A cells in the absence and presence of caffeine inhibited post-replication repair; evidence for an inducible repair mechanism.

The mechanism by which cis-Platinum(II)diamminedichloride, (cis-Pt(II)), inhibited DNA synthesis was investigated using synchronously growing Chinese hamster V79-379A cells. The progression of G1 phase treated cells into S phase was not inhibited. However the rate of DNA synthesis throughout the S phase was depressed in a dose dependent manner compared to a control.

Increased sensitivity of UV-repair-deficient human cells to DNA bound platinum products which unlike thymine dimers are not recognized by an endonuclease extracted from Micrococcus luteus.

We have studied the response of human cells in culture to cis platinum[II] diammine dichloride (cis Pt[II]) induced DNA damage. The survival data, measured as a function of cis Pt[II] dose were similar in a normal cell line (Human foetal lung) compared to a UV-sensitive, thymine dimer excision repair-deficient cell line (Xeroderma pigmentosum). However, there was a marked difference between the two cell lines when binding to DNA was plotted against dose of cis Pt[II] given for 1 h.