Assembly of chloroplast cytochromes b and c.

The synthesis of holocytochromes in plastids is a catalyzed process. Several proteins, including plastid CcsA, Ccs1, possibly CcdA and a thioredoxin, plus at least two additional Ccs factors, are required in sub-stoichiometric amounts for the conversion of apocytochromes f and c(6) to their respective holoforms. CcsA, proposed to be a heme delivery factor, and Ccs1, an apoprotein chaperone, are speculated to interact physically in vivo. The formation of holocytochrome b(6) is a multi-step pathway in which at least four, as yet unidentified, Ccb factors are required for association of the b(H) heme. The specific requirement of reduced heme for in vitro synthesis of a cytochrome b(559)-derived holo-beta(2) suggests that cytochrome b synthesis in PSII might also be catalyzed in vivo.

Induction of coproporphyrinogen oxidase in Chlamydomonas chloroplasts occurs via transcriptional regulation of Cpx1 mediated by copper response elements and increased translation from a copper deficiency-specific form of the transcript.

Coproporphyrinogen III oxidase, encoded by a single nuclear gene in Chlamydomonas reinhardtii, produces three distinct transcripts. One of these transcripts is greatly induced in copper-deficient cells by transcriptional activation, whereas the other forms are copper-insensitive. The induced form of the transcript was expressed coordinately with the cytochrome c6-encoding (Cyc6) gene, which is known to be transcriptionally regulated in copper-deficient cells. The sequence GTAC, which forms the core of a copper response element associated with the Cyc6 gene, is also essential for induction of the Cpx1 gene, suggesting that both are targets of the same signal transduction pathway. The constitutive and induced Cpx1 transcripts have the same half-lives in vivo, and all encode the same polypeptide with a chloroplast-targeting transit sequence, but the shortest one representing the induced form is a 2-4-fold better template for translation than are either of the constitutive forms. The enzyme remains localized to a soluble compartment in the chloroplast even in induced cells, and its abundance is not affected when the tetrapyrrole pathway is manipulated either genetically or by gabaculine treatment.

Stimulation by inositol trisphosphate and tetrakisphosphate of a protein phosphatase.

Several inositol trisphosphate isomers and inositol tetrakisphosphate activate a rat brain phosphoprotein phosphatase, using phosphohistone as well as phosphorylase kinase as substrate. Inositol mono- and bisphosphate have no effect. The protein phosphatase may correspond to type-1 since it is associated with the particulate fraction and is inhibited by heparin. Evidence is presented for the target of inositol phosphate being the catalytic subunit of the protein phosphatase. A parallelism is observed between the ability of the several inositol trisphosphates to activate the protein phosphatase and reported data indicating their ability to release calcium in permeabilized cells.

Mortality and morbidity in pretransplant bilateral nephrectomy: analysis of 305 cases.

The surgical riks were analyzed in 305 patients with end stage renal failure who underwent bilateral nephrectomy through midabdominal approach in preparation for kidney transplantation. The over-all mortality rate was 3.6 per cent. Age was the most significant risk factor in the mortality. Patients less than fifty years of age had an operative mortality rate of 3.1 per cent while those more than fifty years had an operative mortality of 11.1 per cent. Other pertinent risk factors were preoperative complications of renal failure and additional surgical procedures at the time of bilateral nephrectomy. The leading causes of death were those of cardiovascular complications and infection. The morbidity rate was 58.7 per cent being major in 18 per cent and minor in 40.7 per cent. Bilateral nephrectomy is recommended selectively in patients with (1) chronic pyelonephritis with urinary tract infection, (2) major vesicoureteral reflux, (3) immunologically active glomerulonephritis, (4) severe hypertension uncontrollable by adequate dialysis, and (5) extremely large or infected polycystic kidneys.