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PubMed1975

Actinomycin D as the primary agent for gestational trophoblastic disease.

Thirty-one patients with nonmetastatic trophoblastic disease (NMTD) and 39 patients with metastatic trophoblastic disease (MTD) of gestational origin were treated primarily with actinomycin D. Complete and sustained remission was achieved with actinomycin D alone in 94% of patients with NMTD and 67% with MTD. In the nonmetastatic group, 93% of patients without choriocarcinoma (non-CCA) achieved remission with actinomycin D, as compared to 100% (only 3 patients) with CCA. in the metastatic group, 76% of patients without CCA achieved remission with actinomycin D, as compared to 56% where CCA was present. Fourteen of the 15 patients who failed to respond completely to actinomycin D alone subsequently responded to methotrexate (10 patients), triple therapy (3 patients), methotrexate plus triple therapy (1 patient), and methotrexate plus vinblastine (1 patient). One patient died with widespread metastases despite intensive chemotherapy with actinomycin D and triple therapy. No serious toxic side effects were encountered even in treated patients with pre-existing laboratory evidence of impaired hepatic function.

Blood Platelet Disorders↗

PubMed1978

Effects of puromycin and actinomycin D on fertilized rabbit eggs cultured in vitro.

Rabbit zygotes were cultured in media containing varying concentrations of puromycin and actinomycin D in order to determine what effect these agents have on events of fertilization and early development. Concentrations of puromycin greater than 10(-5) M inhibited mitosis, cytokinesis of fertilized eggs and leucine incorporation. In approximately 50% of the zygotes treated with puromycin (10(-5) M or greater) the female pronucleus remained at its site of formation, the cortex, and did not migrate centrad. In these instances the male pronucleus moved from its site of development to the female pronucleus. Concentrations of actinomycin D greater than 10(-7) M also inhibited mitosis and cytokinesis of fertilized eggs. Breakdown of the nuclear envelopes and association of the paternally- and maternally-derived chromatin did not occur in either puromycin- or actinomycin D-treated embryos. Actinomycin D at all of the concentrations employed (10(-9) to 10(-4) M) had little effect upon the structure of nucleolus-like bodies within male and female pronuclei. Male and female pronuclei of puromycin (10(-4) M) and actinomycin D (10(-5) M) treated zygotes, incubated with tritiated thymidine and prepared for scintillation counting and autoradiography, synthesized DNA at a reduced level when compared to control specimens. Although "side effects" of puromycin and actinomycin D treatment are not excluded, these results suggest that nascent proteins may be required for events of fertilization.

Animals↗

PubMedDate not supplied

Actinomycin D binding to unstructured, single-stranded DNA.

Actinomycin D is an anticancer antibiotic best know for inhibiting transcription by binding double-stranded DNA. Tight, sequence selective binding of actinomycin to single-stranded DNA is also known, however, and is implicated in biological activities including inhibition of (-) strand transfer by HIV reverse transcriptase. Oligonucleotide d(GTTAACCATAG) is one of the rare single-stranded DNAs that lack GC steps yet have high affinity for actinomycin. Oligonucleotide sequence and length requirements for drug binding were investigated by monitoring association of the fluorescent surrogate, 7-aminoactinomycin D, to d(GTTAACCATAG) and 31 related oligomers. The TAG-3' terminal sequence was essential for high-affinity binding, but was not sufficient. Five oligomers with TAG sequences on or near the 3'-end had high affinity [K(d) < or = 200 nM (oligomer)]. A sixth oligomer, d(GTAACCATATG), had moderately lower affinity (Kd = 370 nM), and other homologous oligomers had much lower affinity. The minimum length sequence for tight binding of 7-aminoactinomycin D was identified as only eight nucleotides, corresponding to d(AACCATAG). This octanucleotide is unstructured in the absence of actinomycin, and has the highest drug affinity of all oligomers examined (Kd = 125 nM). These studies show that high-affinity binding of 7-aminoactinomycin, and actinomycin D by extension, to single-stranded DNA does not require pre-existing secondary structure or any apparent propensity for secondary structure. It is proposed that actinomycin D binds to certain single-stranded DNA sequences by an induced-fit mechanism favored by participation of at least eight nucleotides, or the equivalent of four base pairs.

Base Sequence↗

PubMed1996

Effects of the transcription inhibitor actinomycin D on postzygotic development of Tetrahymena thermophila conjugants.

During Tetrahymena thermophila conjugation, new somatic macronuclei develop from a common zygotic nucleus derived from meiotic products of the germline, and the old parental somatic nucleus is destroyed. The transcription inhibitor actinomycin D disrupts many events of postzygotic conjugation (cycloheximide causes indistinguishable effects). Early treatment causes a block of all postzygotic development, suggesting a transcription requirement for conjugants to pass a checkpoint, allowing entry into postzygotic development. Thereafter, pair separation, resorption of the old macronucleus, and elimination of one of the new micronuclei are blocked if actinomycin D is added at least 1.5 hr before each of these events normally occurs. Treatment just before DNA rearrangements in the developing macronuclei (anlagen) causes aberrant anlage DNA loss, suggesting that this DNA loss may be caused by inhibition of gene expression involved in genome rearrangements. DNA loss, and correlated lethality, appear to require previous gene expression, since actinomycin D added earlier causes cells to arrest in development without anlage DNA loss, and these conjugants can (at some frequency) complete conjugation and make viable progeny once actinomycin D is removed. The old macronucleus already had been inactivated before most actinomycin D treatments were initiated, indicating that the various induced defects we observed are the result of inhibition of postzygotic gene expression, presumably in anlagen. The defects induced by actinomycin D are similar to defects previously observed in conjugants harboring nullisomic germline deficiencies but proficient old macronuclei.

Animals↗

PubMed1983

Increased uptake of actinomycin D in Ehrlich ascites tumour cells induced by daunorubicin.

The influence of anthracyclines on the uptake of actinomycin D in Ehrlich ascites tumour cells was studied in vitro. The anthracycline daunorubicin significantly increased the [3H]actinomycin D uptake both in whole tumour cells and in isolated nuclei of tumour cells. On the other hand, actinomycin D increased daunorubicin uptake only to a very small degree. Experiments with other intercalating drugs did not influence [3H]actinomycin D binding, suggesting a specific interaction between actinomycin D and the anthracyclines. The mechanism behind this interference is discussed. The increased cellular uptake of actinomycin D in the presence of daunorubicin may have implications for antineoplastic combination chemotherapy.

Animals↗

PubMed1985

Application of 7-amino-actinomycin D for the fluorescence microscopical analysis of DNA in cells and polytene chromosomes.

The cytochemical properties of a guanine-specific synthetic fluorescent analogue of actinomycin D, 7-amino-actinomycin D, have been studied in fixed and living preparations of L cells and polytene chromosomes of salivary glands of Chironomus thummi thummi and Drosophila lummei (Hackman). 7-Amino-actinomycin D has been shown to bind to DNA-containing structures, thereby inducing in them a bright red fluorescence. No specific fluorescence has been found in RNA-containing structures treated with this fluorescent probe. The fluorescence pattern of some regions of polytene chromosomes with a known nucleotide composition was analysed. It has been established that 7-amino-actinomycin D induces a very weak fluorescence in GC-poor chromosome regions of the Drosophila lummei toromere structure. Data indicating a nonlinear dependence between the fluorescence intensity of a stained chromosome region and the GC content in its DNA have been obtained. The influence of DNA nucleotide composition in a chromosome region on the fluorescence of 7-amino-actinomycin D is discussed. In combination with quinacrine staining and the Feulgen fluorescence reaction, treatment with 7-amino-actinomycin D provides useful information about the distribution of GC base pairs in the chromosome region under study.

Animals↗

PubMed1995

Inhibition by actinomycin D of neurogenic mouse ear oedema.

We have investigated the effects of actinomycin D on mouse ear oedema induced by capsaicin, neuropeptides, and established inflammatory mediators. Actinomycin D (0.5 mg/kg, i.v.) significantly (P < 0.01) inhibited ear oedema induced by topical application of capsaicin, while adriamycin (6.0 mg/kg, i.v.) and cycloheximide (6.0 mg/kg, i.v.) had no effect on oedema. The ear oedema induced by intradermal injection of neuropeptides such as mammalian tachykinins, calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP), was markedly (P < 0.05, P < 0.01 or P < 0.001) suppressed by actinomycin D. The drug was also effective (P < 0.01 or P < 0.001) in inhibiting bradykinin (BK)- and compound 48/80-induced ear oedema, but did not inhibit oedema induced by histamine, 5-HT, leukotriene C4 (LTC4), and platelet activating factor (PAF) at a dose of 1 mg/kg. In mast cell-deficient W/WV mice, actinomycin D (1.0 mg/kg, i.v.) failed to inhibit substance P (SP)-induced ear oedema whereas spantide (0.5 mg/kg, i.v.) was an effective (P < 0.01) inhibitor of oedema formation. Furthermore, actinomycin D (10-100 microM) dose-dependently prevented histamine release from rat peritoneal mast cells evoked by SP, compound 48/80, and the ionophore A23182, respectively. These results strongly suggest that an inhibitory effect of actinomycin D on neurogenic inflammation is due primarily to the prevention of mast cell activation mediated by neuropeptides, rather than an interaction with DNA or receptors of neuropeptides.

Animals↗

PubMed2000

Actinomycin D and staurosporine, potent apoptosis inducers in vitro, are potentially effective chemotherapeutic agents against glioblastoma multiforme.

PURPOSE: Although chemotherapeutic protocols that include chloroethylnitrosoureas (CENUs), such as 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and 1, 3-bis(2-chloroethyl)-1-nitrosourea (BCNU), have been a mainstay of treatment for glioblastomas, the clinical outcomes have been unsatisfactory. More effective chemotherapeutic protocols for these tumors will require clear delineation of more cytocidal and cytostatic chemotherapeutic drugs. METHODS AND RESULTS: In this study, we measured the cytocidal effects of ACNU, cisplatin, actinomycin D, and staurosporine, administered within their therapeutic dose ranges, in the treatment of glioblastoma cells. As assessed by WST-1 colorimetric assay, the number of viable cells decreased markedly in T98G cultures treated with actinomycin D or staurosporine, to less than 20% of the level in control cultures at 72 h, but did not decrease or even increased after 6 days of treatment with ACNU. After treatment with cisplatin for 5 days, cell viability decreased to 30% of control. As assessed by fluorescence microscopic examination of nuclear staining by Hoechst 33258 and by electron microscopy, the majority of dead cells treated with actinomycin D, staurosporine, or cisplatin had morphologic features of apoptosis. Caspase-3 activity increased more than 20-fold in cells treated with actinomycin D, staurosporine, or cisplatin but increased less than fivefold in ACNU-treated cells. In addition to caspase-3 activation, western blot analysis demonstrated cleavage of caspase-2 during the apoptotic process. These findings indicate that actinomycin D and staurosporine potently induce apoptosis, whereas ACNU exerts mainly a cytostatic rather than a cytocidal effect. CONCLUSION: Actinomycin D and staurosporine and their derivatives are potentially effective chemotherapeutic agents against glioblastoma cells at least in vitro.

Antibiotics, Antineoplastic↗

PubMed1985

Actinomycin D-associated lesions mimicking DNA-DNA interstrand crosslinks detected by alkaline elution in cultured mammalian cells.

Cultured human fibroblasts were exposed to various concentrations of actinomycin D, a DNA intercalating agent, and studied by various alkaline elution techniques for the presence of DNA lesions. DNA-protein crosslinks increased proportionately with increasing actinomycin D, with 1.53 crosslinks/10(6) nucleotides after 5 micrograms/ml exposure. However, in the single-strand DNA break assay, elution of DNA initially increased as expected with increasing actinomycin D but thereafter decreased, with only 0.09 breaks/10(6) nucleotides detected after 25 micrograms/ml exposure, suggesting the presence of DNA crosslinking. A standard alkaline elution assay for DNA-DNA crosslinking was performed, and lesions which mimicked such crosslinks were detected, with a relative crosslink frequency of 2.30 after 5 micrograms/ml exposure. These actinomycin D-associated lesions disappeared when the alkaline elution procedure was modified to include additional proteinase digestion and use of the detergent sodium dodecyl sulfate (SDS) in the elution buffer, suggesting that they represented undigested DNA-protein crosslinks or nonspecific protein on the filters inhibiting DNA elution. Greater than ten times as many DNA-protein crosslinks were detected in fibroblasts than the number of single-strand DNA breaks after cellular exposure to actinomycin, even after determining breaks using the modified methodology for decreasing cellular protein interference. The data suggest that the actinomycin-DNA complex is associated with the formation of DNA-protein crosslinks which represent lesions other than endonuclease-associated DNA strand scission.

Cells, Cultured↗

PubMed1991

Modulation of the reversibility of actinomycin D cytotoxicity in HeLa cells by verapamil.

Actinomycin D treatment (0.001-0.005 micrograms/ml; 0.5-24 h) induced a dose and time response shifting of nucleolar to nuclear fluorescence. In the presence of verapamil, cells were more responsive to actinomycin D. Translocation of protein B23 occurred with lower doses of actinomycin D and in shorter incubation times in the presence of verapamil. Short exposure (0.5 h) of HeLa cells to actinomycin D (0.05-0.25 micrograms/ml) induced 'reversible' translocation of protein B23 as well as 'reversible' inhibition of cell growth and RNA synthesis. Verapamil (5 microM) included in the cell culture after removal of actinomycin D inhibited the recoveries of cell growth, RNA synthesis as well as the corresponding relocalization of protein B23 from the nucleoplasm to nucleoli. These results indicate that verapamil can potentiate the antiproliferating activity of actinomycin D by inhibiting reversibility of its cytotoxicity and suggest clinical application.

Cell Division↗

PubMed1999

Actinomycin D as a novel SH2 domain ligand inhibits Shc/Grb2 interaction in B104-1-1 (neu*-transformed NIH3T3) and SAA (hEGFR-overexpressed NIH3T3) cells.

Actinomycins, a family of bicyclic chromopeptide lactones with strong antineoplastic activity, were screened as inhibitors of Shc/Grb2 interaction in in vitro assay systems. To investigate the effects of actinomycin D on Shc/Grb2 interaction in cell-based experiments, we used SAA (normal hEGFR-overexpressed NIH3T3) cells and B104-1-1 (neu*-transformed NIH3T3) cells, because a large number of the Shc/Grb2 complexes were detected. Associated protein complexes containing Shc were immunoprecipitated from actinomycin D-treated cell lysates with polyclonal anti-Shc antibody. Then the association with Grb2 was assessed by immunoblotting with monoclonal anti-Grb2 antibody. The result of the immunoblotting experiment revealed that actinomycin D inhibited Shc/Grb2 interaction in a dose-dependent manner in both B104-1-1 and EGF-stimulated SAA cells. The inhibition of Shc/Grb2 interaction by actinomycin D in B104-1-1 cells also reduced tyrosine phosphorylation of MAP kinase (Erk1/Erk2), one of the major components in the Ras-MAP kinase signaling pathway. These results suggest that actinomycin D could be a non-phosphorylated natural and cellular membrane-permeable SH2 domain antagonist.

Adaptor Proteins, Signal Transducing↗

PubMed1997

Actinomycin D treatment leads to differentiation and inhibits proliferation in rhabdomyosarcoma cells.

Human embryonal cell line RD is derived from rhabdomyosarcoma, a tumor of childhood that arises from rhabdomyoblasts probably arrested somewhere along their pathway to maturation. Because actinomycin D is a drug of choice in the treatment of rhabdomyosarcomas, and because it has been used to induce differentiation as an alternative therapy for myeloproliferative syndromes, we treated RD cells with different concentrations of actinomycin D and evaluated the effects on growth and differentiation. Actinomycin D treatment in vitro caused time- and dose-dependent growth inhibition. Interestingly, RD cells treated with low doses (2.85 and 5.7 nmol/L) of actinomycin D for 6 days showed morphologic and phenotypic differentiation, with increased expression of desmin, alpha-actinin, and tropomyosin. However, treatment with 11.4 nmol/L actinomycin D strongly inhibited growth and had cytotoxic effects that prevented the cells from attaining myogenic differentiation. We conclude that exposure of this human embryonal rhabdomyosarcoma cell line to low concentrations of actinomycin D released the neoplastic cells from their blockade, allowing them to recover normal myogenic development. We suggest a potential role for differentiation therapy in the treatment of rhabdomyosarcomas.

Antibiotics, Antineoplastic↗

PubMed1982

Adjuvant vinblastine, actinomycin D, bleomycin, cyclophosphamide and cis-platinum chemotherapy regimen with and without maintenance in patients with resected stage IIB testis cancer.

A total of 42 patients with stage IIB nonseminomatous germ cell tumors of the testis after orchiectomy and retroperitoneal lymph node dissection received adjuvant chemotherapy with the modified vinblastine, actinomycin D, bleomycin, cyclophosphamide and cis-platinum regimen. Of the patients 29 had N2B and 13 had N3 nodal categories. Adjuvant vinblastine, actinomycin D, bleomycin, cyclophosphamide and cis-platinum chemotherapy was given with maintenance in the first 24 patients and without maintenance (2 months of chemotherapy) in the subsequent 18. Chemotherapy with maintenance was given for 1 year and began with 2 inductions 3 to 4 weeks apart: 600 mg./m.2 intravenous cyclophosphamide, 30 mg. intravenous bleomycin, 1 mg./m.2 intravenous actinomycin D and 4 mg./m.2 intravenous vinblastine on day 1, 20 mg./m.2 bleomycin daily by continuous 24-hour induction on days 1 to 3 and 120 mg./m.2 intravenous cis-platinum with mannitol-induced diuresis on day 4. Maintenance with 6 mg./m.2 intravenous vinblastine and 1 mg./m.2 intravenous actinomycin D every 3 weeks was initiated 3 weeks after the second induction for the remainder of the year. Adjuvant vinblastine, actinomycin D, bleomycin, cyclophosphamide and cis-platinum chemotherapy without maintenance was given for 2 months and used 3 inductions identical to those described previously. Complete remission has been maintained in 41 of 42 patients: all 24 who received maintenance chemotherapy and 17 of 18 who did not. One patient had a relapse with sarcoma and 6 required broad-spectrum antibiotics for fever during myelosuppression. A temporary increase in the serum creatinine of more than 2 mg. per cent occurred in 1 patient. Chronic renal failure or pulmonary fibrosis was not seen. Our results show that vinblastine, actinomycin D, bleomycin, cyclophosphamide and cis-platinum chemotherapy is effective in the prevention of recurrences in patients with resected stage IIB disease, and suggest that adjuvant chemotherapy is equally effective with or without maintenance.

Adolescent↗

PubMed1996

Sequence-specific actinomycin D binding to single-stranded DNA inhibits HIV reverse transcriptase and other polymerases.

Primer extension assays using recombinant templates constructed to contain all 256 possible base quartets in a minimum length sequence were used to examine binding of the anticancer drug actinomycin D to single-stranded DNA. Single-stranded templates were generated by digestion of linearized plasmid with the double-strand-specific T7 gene 6 exonuclease. Actinomycin D formed high-affinity, kinetically stable complexes that paused primer elongation at specific sites by HIV-1 reverse transcriptase, Sequenase (modified T4 DNA polymerase), the Klenow fragment of Escherichia coli DNA polymerase, and Vent (exo-) DNA polymerase. Pauses occurred most commonly near G+C-rich nucleotide clusters, including GpC steps, the preferred sites of double-stranded DNA binding. Complexes were stable for several minutes at temperatures over 50 degrees C as determined by their abilities to pause Vent polymerase at elevated temperatures. Significant variations were noted in pause patterns of different polymerases, demonstrating differential responses of polymerases to a bound actinomycin. Covalent adducts formed on template DNA by a photoaffinity analog of actinomycin D completely stopped primer extension. These results support the possibility that actinomycin D inhibits transcription elongation by complexing single-stranded DNA in the open transcription complex. Single-stranded DNA binding by actinomycin D or analogs may also provide routes for combating HIV or other viruses which replicate through single-stranded intermediates.

Base Composition↗

PubMed1983

Tetracyclic chromophoric analogues of actinomycin D: synthesis, structure elucidation and interconvertibility from one form to another, antitumor activity, and structure-activity relationships.

Two different tetracyclic chromophoric analogues of actinomycin D have been synthesized by engaging two chromophoric DNA-binding functions in actinomycin D, i.e., 2-amino and 3-oxo, into either a 1,4-oxazin-2-one or an oxazole ring system. A third analogue has an extra quinone function at C-8 of the oxazole analogue. In all the analogues the chemical integrity of the peptide lactones of the parent antibiotic is kept intact, but their sterochemistry is altered. The analogues are designed as transport-modified prodrug forms of either the tricyclic active analogues of actinomycin D or actinomycin D itself. All analogues exhibit cytotoxicity that is several-fold less potent than AMD; they also have no binding affinity toward extracellular DNA. Nonetheless, the analogues of the first and the third series show improved antitumor activities (P388 leukemia, CDF1 mice). In fact, two of these analogues having a phenyl substituent at the C-3 site of the oxazinone ring or the C-2 position of the 8-oxo-8H-oxazole ring exhibit the highest antitumor effects. Most of the analogues are active over a broader dose range than actinomycin D and are 6- to 16-fold less cytotoxic to human lymphoblastic leukemia (CCFR-CEM) cells in vitro. The analogues with the most pronounced antitumor activity are those that retain most elements in the peptide stereochemistry of actinomycin D and have a quinone function or demonstrate susceptibility of their chromophores to biotransformation.

Animals↗

PubMed1969

A study of nucleolar vacuoles in cultured tobacco cells using radioautography, actinomycin D, and electron microscopy.

Previously it has been found that in tobacco callus cells nucleolar vacuoles repeatedly form and contract. In this study, nucleolar vacuoles were investigated by using radioautography, actinomycin D, and electron microscopy. It was found, from grain counts of nucleoli labeled with uridine-(3)H, that nucleoli containing vacuoles had more than three times as many grains/micro(2) of nucleolar substance as did nucleolei without vacuoles. Treatment of tobacco callus cells with various concentrations of actinomycin D caused the percentage of cells containing nucleolar vacuoles to decrease; with the highest concentration the percentage of these cells dropped from the normal level of about 70% to less than 10%. However, after removal of actinomycin D the cells regained nucleolar vacuoles up to the control level. When radioautography was used with actinomycin D, it was found that the actinomycin D inhibited the uptake of uridine-(3)H, i.e. inhibited RNA synthesis, in those nucleoli which lost their nucleolar vacuoles. In addition, after removal of the cells from actinomycin D, it was found that as the cells regained nucleolar vacuoles the nucleoli also began to incorporate uridine-(3)H. Electron micrographs showed the nucleoli to be composed of a compact, finely fibrous central portion surrounded by a layer of dense particles 100-150 A in diameter. Nucleolar vacuoles occurred in the fibrous central portion. Dense particles similar to those in the outer layer of the nucleoli were found scattered throughout the vacuoles and in a dense layer at their outer edge. These data suggest that in cultured tobacco callus cells the formation and contraction of nucleolar vacuoles is closely related to RNA synthesis in the nucleolus.

Autoradiography↗

PubMed1995

Phase I study of tumor necrosis factor plus actinomycin D in patients with androgen-independent prostate cancer.

Based on preclinical studies which reveal enhanced antitumor activity of tumor necrosis factor (TNF) when combined with actinomycin D in human prostate cancer cell lines, we performed a phase I clinical study combining TNF and actinomycin D. All patients had metastatic prostatic carcinoma exhibiting androgen-independent growth. Patients were treated with a combination of a short infusion of actinomycin D followed by a TNF infusion daily for five consecutive days. Soluble TNF receptor p60 was not modulated by treatment but p80 receptor increased significantly following treatment with a combination of TNF and actinomycin D (baseline median 3.4 ng/ml) range 2.5-6.6 ng/ml follow up (9.3 ng/ml) range 6-24 ng/ml. We concluded that the maximum tolerated dose of continuous infusion TNF and short infusion actinomycin D is 400 micrograms/m2 of actinomycin D and 400 micrograms/m2 of TNF. The increased soluble receptor isoform (p80) may account for the lack of clinical activity seen in this trial. Should these results be confirmed, a strategy focused on overcoming the upregulation of the TNF soluble receptor will be required before further study of TNF should be considered.

Aged↗

PubMed1978

Origin of the actinomycin D insensitive RNA species in Aedes albopictus cells.

In the presence of actinomycin D or a combination of actinomycin D and either camptothecin or alpha-amanatin. Aedes albopictus cells synthesize a variety of single stranded RNA species. These actinomycin D resistant species are ethidium bromide sensitive and they are present in the cell cytoplasm in an RNase resistant structure which has the sedimentation and buoyant density characteristics of mitochondria. Twelve actinomycin D insensitive RNA species can be detected by electrophoresis in 7M urea and 11 of these bind to oligo(dT)-cellulose. An identical set of oligo(dT)-cellulose binding RNA species is obtained when A. albopictus cells are labeled in the presence of camptothecin alone. The actinomycin D insensitive RNA species which bind to oligo(dT)-cellulose hybridize to mitochondrial DNA. These data indicate that the actinomycin D insensitive RNA species have a mitochondrial origin and are not associated with the replication of an inapparent contaminating virus.

Aedes↗