Studies on ethnomedicinal plants used by the Malayali tribe of Kalrayan Hill, Tamil Nadu state

An ethnomedicinal plants survey was carried out to collect the information about themedicinal plants found in kalrayan hill and used by the native malayali tribe of SouthernEastern Ghats of India. 80 plant species, belonging to 41 families, which are used intraditional health care system are described under this study. The studies also attempted tofind out the medicines prepared out of these medicinal plants, forms of medicine and theircorresponding ailments. In this communication, the information obtained from the tribalswas compared with the already existing literatures on ethnobotany of India. The documentedethnomedicinal plants were mostly used to cure skin diseases, wounds and rheumatism. Themedicinal plants used by the tribals are arranged alphabetically, and followed by theirbotanical name, family name, common names, vernacular name(s), part(s) used, mode ofpreparation and their corresponding diseases

Traditional Phytotherapy for Diabetes Used by the People of Perambalur District, Tamilnadu, South India

Diabetes is caused due to deficiency in production of insulin by the pancreas, or by the ineffectiveness of the insulin produced. It is a global problem and the numbers of people affected are increasing day by day. Plants provide a potential source of antidiabetic drugs. In India, most of the people, especially in rural areas use traditional medicine of plants to treat many diseases including diabetes. The aim of the present study was to document medicinal plants, traditionally used to treat diabetes by the people of Perambalur district. Traditional health practitioners were interviewed with standardized questionnaires in order to obtain information on medicinal plants traditionally used for the management of diabetes. Thirty species of 29 genera and 22 families were encountered during this study

Isozyme studies of resistant and susceptible clones of Saccharum officinarum L. to fungal diseases

Sugarcane is one of the important commercial crops of India and it plays an important role in maintaining the economy of the nation. Many diseases of sugarcane lead to loss of net productivity of sugar and by growing resistant varieties the loss can be reduced to considerable amount. Hence, in this study an attempt has been made to identify a resistant clone through isoenzyme analysis. Three resistant (Bo-91, Co-86249, Co-93009) and three susceptible (CoC-671, CoC-86032, CoC-92061) clones of Saccharum officianarum L. were selected for the study. In native-PAGE analysis (for peroxidase) distinct bands with Rf value 0.537 and 0.694 were observed in resistant clones, and the susceptible clones lack these bands.  An increase in peroxidase activity is also observed in clones that possessed the distinct Rf values 0.537 and 0.694. From this, it can be concluded that the clones possessing distinct Rf values are resistants when compared to other clones as they are having high peroxidase action

Agrobacterium mediated Transformation of rice, var. Pusa Basmati-1

The present study was aimed at the Agrobacterium mediated transformation of rice (Oryza sativa L.) variety Pusa Basmati-1 .Agrobacterium tumefaciens strain LBA 4404 harboring the binary vector (pIG121) that carries the genes for ß-glucuronidase and hygromycin phosphotransferase (hpt) was used for transformation. Co-cultured calli were undergone for GUS histochemical analysis of transformed calli and followed by molecular analysis by using PCR to confirm the presence of transgenes

Impact of histone H4 lysine 20 methylation on 53BP1 responses to chromosomal double strand breaks.

Recruitment of 53BP1 to chromatin flanking double strand breaks (DSBs) requires γH2AX/MDC1/RNF8-dependent ubiquitination of chromatin and interaction of 53BP1 with histone H4 methylated on lysine 20 (H4K20me). Several histone methyltransferases have been implicated in 53BP1 recruitment, but their quantitative contributions to the 53BP1 response are unclear. We have developed a multi-photon laser (MPL) system to target DSBs to subfemtoliter nuclear volumes and used this to mathematically model DSB response kinetics of MDC1 and of 53BP1. In contrast to MDC1, which revealed first order kinetics, the 53BP1 MPL-DSB response is best fitted by a Gompertz growth function. The 53BP1 MPL response shows the expected dependency on MDC1 and RNF8. We determined the impact of altered H4K20 methylation on 53BP1 MPL response kinetics in mouse embryonic fibroblasts (MEFs) lacking key H4K20 histone methyltransferases. This revealed no major requirement for the known H4K20 dimethylases Suv4-20h1 and Suv4-20h2 in 53BP1 recruitment or DSB repair function, but a key role for the H4K20 monomethylase, PR-SET7. The histone methyltransferase MMSET/WHSC1 has recently been implicated in 53BP1 DSB recruitment. We found that WHSC1 homozygous mutant MEFs reveal an alteration in balance of H4K20 methylation patterns; however, 53BP1 DSB responses in these cells appear normal

PARP3 affects the relative contribution of homologous recombination and nonhomologous end-joining pathways

The repair of toxic double-strand breaks (DSB) is critical for the maintenance of genome integrity. The major mechanisms that cope with DSB are: homologous recombination (HR) and classical or alternative nonhomologous end joining (C-NHEJ versus A-EJ). Because these pathways compete for the repair of DSB, the choice of the appropriate repair pathway is pivotal. Among the mechanisms that influence this choice, deoxyribonucleic acid (DNA) end resection plays a critical role by driving cells to HR, while accurate C-NHEJ is suppressed. Furthermore, end resection promotes error-prone A-EJ. Increasing evidence define Poly(ADP-ribose) polymerase 3 (PARP3, also known as ARTD3) as an important player in cellular response to DSB. In this work, we reveal a specific feature of PARP3 that together with Ku80 limits DNA end resection and thereby helps in making the choice between HR and NHEJ pathways. PARP3 interacts with and PARylates Ku70/Ku80. The depletion of PARP3 impairs the recruitment of YFP-Ku80 to laser-induced DNA damage sites and induces an imbalance between BRCA1 and 53BP1. Both events result in compromised accurate C-NHEJ and a concomitant increase in DNA end resection. Nevertheless, HR is significantly reduced upon PARP3 silencing while the enhanced end resection causes mutagenic deletions during A-EJ. As a result, the absence of PARP3 confers hypersensitivity to anti-tumoral drugs generating DSB

LRF maintains genome integrity by regulating the non-homologous end joining pathway of DNA repair

Leukemia/lymphoma-related factor (LRF) is a POZ/BTB and Krüppel (POK) transcriptional repressor characterized by context-dependent key roles in cell fate decision and tumorigenesis. Here we demonstrate an unexpected transcription-independent function for LRF in the classical non-homologous end joining (cNHEJ) pathway of double-strand break (DSB) repair. We find that LRF loss in cell lines and mouse tissues results in defective cNHEJ, genomic instability and hypersensitivity to ionizing radiation. Mechanistically, we show that LRF binds and stabilizes DNA-PKcs on DSBs, in turn favouring DNA-PK activity. Importantly, LRF loss restores ionizing radiation sensitivity to p53 null cells, making LRF an attractive biomarker to direct p53-null LRF-deficient tumours towards therapeutic treatments based on genotoxic agents or PARP inhibitors following a synthetic lethal strategy

Complex Breakpoints and Template Switching Associated with Non-canonical Termination of Homologous Recombination in Mammalian Cells

A proportion of homologous recombination (HR) events in mammalian cells resolve by “long tract” gene conversion, reflecting copying of several kilobases from the donor sister chromatid prior to termination. Cells lacking the major hereditary breast/ovarian cancer predisposition genes, BRCA1 or BRCA2, or certain other HR-defective cells, reveal a bias in favor of long tract gene conversion, suggesting that this aberrant HR outcome might be connected with genomic instability. If termination of gene conversion occurs in regions lacking homology with the second end of the break, the normal mechanism of HR termination by annealing (i.e., homologous pairing) is not available and termination must occur by as yet poorly defined non-canonical mechanisms. Here we use a previously described HR reporter to analyze mechanisms of non-canonical termination of long tract gene conversion in mammalian cells. We find that non-canonical HR termination can occur in the absence of the classical non-homologous end joining gene XRCC4. We observe obligatory use of microhomology (MH)-mediated end joining and/or nucleotide addition during rejoining with the second end of the break. Notably, non-canonical HR termination is associated with complex breakpoints. We identify roles for homology-mediated template switching and, potentially, MH-mediated template switching/microhomology-mediated break-induced replication, in the formation of complex breakpoints at sites of non-canonical HR termination. This work identifies non-canonical HR termination as a potential contributor to genomic instability and to the formation of complex breakpoints in cancer

Complex Breakpoints and Template Switching Associated with Non-canonical Termination of Homologous Recombination in Mammalian Cells.

A proportion of homologous recombination (HR) events in mammalian cells resolve by "long tract" gene conversion, reflecting copying of several kilobases from the donor sister chromatid prior to termination. Cells lacking the major hereditary breast/ovarian cancer predisposition genes, BRCA1 or BRCA2, or certain other HR-defective cells, reveal a bias in favor of long tract gene conversion, suggesting that this aberrant HR outcome might be connected with genomic instability. If termination of gene conversion occurs in regions lacking homology with the second end of the break, the normal mechanism of HR termination by annealing (i.e., homologous pairing) is not available and termination must occur by as yet poorly defined non-canonical mechanisms. Here we use a previously described HR reporter to analyze mechanisms of non-canonical termination of long tract gene conversion in mammalian cells. We find that non-canonical HR termination can occur in the absence of the classical non-homologous end joining gene XRCC4. We observe obligatory use of microhomology (MH)-mediated end joining and/or nucleotide addition during rejoining with the second end of the break. Notably, non-canonical HR termination is associated with complex breakpoints. We identify roles for homology-mediated template switching and, potentially, MH-mediated template switching/microhomology-mediated break-induced replication, in the formation of complex breakpoints at sites of non-canonical HR termination. This work identifies non-canonical HR termination as a potential contributor to genomic instability and to the formation of complex breakpoints in cancer