Biology subjects

Maldonado, L.

Publications and source records attributed to Maldonado, L..

3 recordsLinked to original sources

bioRxiv2025

Phylogeny and chromosomal differentiation in Cestreae (Solanaceae)

Cestreae is a monophyletic tribe within the subfamily Cestroideae (Solanaceae), comprising the American genera Cestrum, Sessea, and Vestia. While the monophyly of Cestrum has been confirmed by DNA sequences, the phylogenetic relationships among its species, as well as its relationship to Sessea and Vestia remain unresolved. This study describes cytogenetic traits, expands cytological records, extends phylogenetic sampling, and analyzes chromosome evolution in Cestreae through ancestral character reconstruction. Chromosome counts, karyotype analyses, and B chromosome identification were conducted using root meristem preparations stained with Giemsa. Fluorescent in situ hybridization (FISH) with rDNA probes and DAPI was used to examine rDNA distribution. Phylogenetic relationships were inferred for 23 species using four molecular markers (ITS, matK, ndhF, and trnL-F) under Maximum Likelihood and Bayesian Inference approaches. In addition to sequences from GenBank/NCBI, 14 ITS new sequences were obtained from PCR products. Ancestral haploid chromosome numbers (n) were reconstructed using ChromEvol, while karyotype formulae and rDNA distribution patterns were inferred through stochastic character mapping (SCM) in R. All analyzed species had a chromosome number of 2n = 16, with two types of karyotype formula. Three Cestrum species possessed B chromosomes, and four distinct rDNA distribution patterns were identified. Ancestral state reconstruction suggests that 2n = 16, a karyotype formula of 7m + 1sm, and rDNA synteny (18-5.8-26S + 5S) on sm pair #8 and terminal 18-5.8-26S sites on one m chromosome pair, may represent ancestral characteristics in Cestreae.

evolutionary biology↗

bioRxiv2020

Molecular features similarities between SARS-CoV-2, SARS, MERS and key human genes could favour the viral infections and trigger collateral effects

In December 2019 rising pneumonia cases caused by a novel {beta}-coronavirus (SARS-CoV-2) occurred in Wuhan, China, which has rapidly spread worldwide causing thousands of deaths. The WHO declared the SARS-CoV-2 outbreak as a public health emergency of international concern therefore several scientists are dedicated to the study of the new virus. Since human viruses have codon usage biases that match highly expressed proteins in the tissues they infect and depend on host cell machinery for replication and co-evolution, we selected the genes that are highly expressed in the tissue of human lungs to perform computational studies that permit to compare their molecular features with SARS, SARS-CoV-2 and MERS genes. In our studies, we analysed 91 molecular features for 339 viral genes and 463 human genes that consisted of 677873 codon positions. Hereby, we found that A/T bias in viral genes could propitiate the viral infection favoured by a host dependant specialization using the host cell machinery of only some genes. The envelope protein E, the membrane glycoprotein M and ORF7 could have been further benefited by a high rate of A/T in the third codon position. Thereby, the mistranslation or de-regulation of protein synthesis could produce collateral effects, as a consequence of viral occupancy of the host translation machinery due tomolecular similarities with viral genes. Furthermore, we provided a list of candidate human genes whose molecular features match those of SARS-CoV-2, SARSand MERS genes, which should be considered to be incorporated into genetic population studies to evaluate thesusceptibility to respiratory viral infections caused by these viruses. The results presented here, settle the basis for further research in the field of human genetics associated with the new viral infection, COVID-19, caused by SARS-CoV-2 and for the development of antiviral preventive methods.

genomics↗

bioRxiv2019

Allele-specific DNA methylation is increased in cancers and its dense mapping in normal plus neoplastic cells increases the yield of disease-associated regulatory SNPs

BackgroundMapping of allele-specific DNA methylation (ASM) can be a post-GWAS strategy for localizing regulatory sequence polymorphisms (rSNPs). However, the advantages of this approach, and the mechanisms underlying ASM in normal and neoplastic cells, remain to be clarified. ResultsWe performed whole genome methyl-seq on diverse normal cells and tissues and three types of cancers (multiple myeloma, lymphoma, glioblastoma multiforme). After excluding imprinting, the data pinpointed 15,114 high-confidence ASM differentially methylated regions (DMRs), of which 1,842 contained SNPs in strong linkage disequilibrium or coinciding with GWAS peaks. ASM frequencies were increased 5 to 9-fold in cancers vs. matched normal tissues, due to widespread allele-specific hypomethylation and focal allele-specific hypermethylation in poised chromatin. Cancers showed increased allele switching at ASM loci, but disruptive SNPs in specific classes of CTCF and transcription factor (TF) binding motifs were similarly correlated with ASM in cancer and non-cancer. Rare somatic mutations affecting these same motif classes tracked with de novo ASM in the cancers. Allele-specific TF binding from ChIP-seq was enriched among ASM loci, but most ASM DMRs lacked such annotations, and some were found in otherwise uninformative "chromatin deserts". ConclusionsASM is increased in cancers but occurs by a shared mechanism involving disruptive SNPs in CTCF and TF binding sites in both normal and neoplastic cells. Dense ASM mapping in normal plus cancer samples reveals candidate rSNPs that are difficult to find by other approaches. Together with GWAS data, these rSNPs can nominate specific transcriptional pathways in susceptibility to autoimmune, neuropsychiatric, and neoplastic diseases. Custom genome browser tracks with annotated ASM loci can be viewed at a UCSC browser session hosted by our laboratory (https://bit.ly/tycko-asm)

genomics↗