ISSN / EISSN : 23257776 / 23257792
Current Publisher: Scientific Research Publishing, Inc. (10.4236)
Total articles ≅ 70
Latest articles in this journal
CellBio, Volume 9, pp 29-84; doi:10.4236/cellbio.2020.91003
It is believed that eukaryotes arise from prokaryotes, which means that organelles can form de novo in prokaryotes. Such events, however, had not been observed previously. Here, we report the biogenesis of orga-nelles in the endosymbiotic cyanobacterium TDX16 (prokaryote) that was released from its senescent/necrotic host cell of green alga Haema-tococcus pluvialis (eukaryote). Microscopic observations showed that organelle biogenesis in TDX16 initiated with cytoplasm compartmental-ization, followed by de-compartmentalization, DNA allocation, and re-compartmentalization, as such two composite organelles-the primi-tive chloroplast and primitive nucleus sequestering minor and major fractions of cellular DNA respectively were formed. Thereafter, the eu-karyotic cytoplasmic matrix was built up from the matrix extruded from the primitive nucleus; mitochondria were assembled in and segregated from the primitive chloroplast, whereby the primitive nucleus and primi-tive chloroplast matured into the nucleus and chloroplast respectively. While mitochondria subsequently turned into double-membraned vacu-oles after matrix degradation. Results of pigment analyses, 16S rRNA and genome sequencing revealed that TDX16 is a phycocyanin-containing cyanobacterium resembling Chroococcidiopsis thermalis, which had ac-quired 9,017,401 bp DNAs with 10,301 genes from its host. Accordingly, we conclude that organelle biogenesis in TDX16 is achieved by hybridiz-ing the acquired eukaryotic DNAs with its own one and expressing the hybrid genome. The formation of organelles in cyanobacterium TDX16 is the first case of organelle biogenesis in prokaryotes observed so far, which sheds an unprecedented light on eukaryotes and their connections with prokaryotes, and thus has broad implications on biology.
CellBio, Volume 9, pp 14-28; doi:10.4236/cellbio.2020.91002
While micronuclei (MN) store extranuclear DNA and cause genome instability, the effects of nuclear envelope (NE) assembly defects associated with MN on genome instability remain largely unknown. Here, we investigated the NE protein distribution in MN using HeLa human cervical cancer cells. Under the standard condition and two pharmacological culture conditions, we found that three types of NE protein assemblies were associated with MN: 1) intact NE assembly, in which both core and non-core NE proteins were evenly present; 2) type I assembly, in which only core NE proteins were detectable; and 3) type II assembly in which a region deficient for both core and non-core NE proteins existed and a pattern recognition receptor, cyclic guanosine monophos-phate-adenosine monophosphate synthase, was frequently detected. Our findings provide experimental settings and a method of grouping MN-associated NE defects, which may be helpful for researchers who are interested in regulation of genome and nuclear organization relevant to cancer development.
CellBio, Volume 9, pp 1-13; doi:10.4236/cellbio.2020.91001
Cell fleeing from death phenomenon occurs as either complete or incomplete; the phenomenon is incomplete fleeing from death when cell blocks intrinsic death program only. But, it becomes complete fleeing from death if the cell successfully blocks the pathway of intrinsic and extrinsic programs of cell death. This phenomenon is induced by the formation of hydrogen peroxide which activates nuclear factor kappa B. The nuclear factor-kappa B stimulates the expression of several genes, to produces 6 factors (BcL-2, Muc-1, MMPs, DcR3, Muc-4, muc-16, and TNF-α). Such factors act as blockers of the pathway of intrinsic and extrinsic programs of cell death. These blockers convert normal cell to a cancer cell. If these blockers are removed, the death programs of cancer cells will run again and cancer will disappear.
CellBio, Volume 8, pp 41-51; doi:10.4236/cellbio.2019.83003
The ultrastructure of apical meristem cells was studied in Triticum aestivum L. cv. “Trizo” seedlings grown on soil without or enriched with selenium and survived 14 days’ stress caused by lead pollution in the soil. The soil treatments: control—the original soil; (Pb1)—50 mg·kg−1; (Pb2)—100 mg·kg−1; (Pb1 + Se1) —0.4 mg·kg−1 Se added to Pb1 treated soil; (Pb1 + Se2)—0.8 mg·kg−1 Se added to Pb1 treated soil; (Pb2 + Se1)—0.4 mg·kg−1 Se added to Pb2 treated soil; (Pb2 + Se2)—0.8 mg·kg−1 Se added to Pb2 treated soil were used. Light and other conditions were optimal for plant growth. A distinctive feature of the cells of the apical meristem of control plants was the absence of nuclear membranes. Proplastids were membrane vesicles 1 - 2 microns in diameter, filled with contents of varying degrees of density, from membrane vesicles containing only plastid DNA up to a fully formed structure of proplastids. In (Pb1)-plants, the amount of cytoplasmic ribosomes and proplastids in the meristematic cells was less than in the control. The structure of the forming proplastids was almost the same as that of the control plants. Signs of degradation of meristematic proplastids, such as a decrease of their diameter, observed in (Pb2)-plants. The introduction of selenium into lead contaminated soil increased the accumulation of Pb in plants, especially in the roots and apical meristem. In (Pb1 + Se1)-, (Pb1 + Se2)-, (Pb2 + Se1)-, and (Pb2 + Se2)-plants, the number of cytoplasmic ribosomes in meristematic cells increased, which indirectly indicates an increase in protein synthesis. Based on our concept about the formation (assembly) of proplastids in the cells of the apical meristem, we believe that toxic agents, such as lead, which inhibit the development of proplastids into chloroplasts in mesophyll cells, act on apical meristem cells at the stage when plastid DNA is replicated in the cytoplasm and is not yet surrounded by a plastid membrane.
CellBio, Volume 8, pp 17-39; doi:10.4236/cellbio.2019.82002
Cancer is cell fleeing from death by blocking the intrinsic and extrinsic pathways of cell death programs. In the present work, the experimental formula was designed to remove these blockers. It was applied on 120 Swiss albino mice which were inoculated intraperitoneally and subcutaneously with Ehrlich Ascites Carcinoma cells; 1 × (106) cell/mouse. The activity of the cell death programs of the tumor was detected by measuring the volume of Ascites fluid, counting the number of dead cancer cells, measuring the size of the tumor, detecting the positive reaction of caspase enzyme in cancer cells and presence of macrophages and apoptotic bodies in tumor tissue. The experimental formula succeeded in removing the blockers of the cell death program in cancer cells returning the cell death program to work again.
CellBio, Volume 8, pp 53-65; doi:10.4236/cellbio.2019.84004
Cypermethrin (Cym) is a synthetic class II pyrethroid that is widely used and has a big risk to health. Cypermethrin produces oxidative stress and enhances inflammatory damage of liver. The present study was designed to investigate the ameliorating effects of NSe against Cym-induced hepatotoxicity in rats. For this purpose, twenty four male rats were divided into three groups. Group (I) was gavaged with Cym (control group), group (II) gavaged daily with Cym (1 mg/kg body weight), and group (III) gavaged with Cym + NSe (2.5 mg kg body weight/day, three times a week) for 21 days. Cypermethrin increased serum liver enzymes, oxidative stress and inflammatory markers. Administration of NSe significantly reduced the increased serum liver enzymes and inflammatory parameters and restored the antioxidant capacity in liver. Our results suggest that Nse exhibits promising hepato-protective effects against Cym-induced oxidative damage and inflammation.
CellBio, Volume 8, pp 1-16; doi:10.4236/cellbio.2019.81001
CellBio, Volume 7, pp 23-34; doi:10.4236/cellbio.2018.72003
CellBio, Volume 7, pp 1-11; doi:10.4236/cellbio.2018.71001
CellBio, Volume 8, pp 13-22; doi:10.4236/cellbio.2018.82002