Genetic, environmental and microbiological causes of periodontal diseases

Periodontal disease is a term that can be used to describe different oral conditions that occur to the gingiva, in addition to the bones and ligaments supporting the teeth. Periodontal diseases can develop secondary to inflammatory, developmental, genetic, traumatic, neoplastic, and metabolic disorders. In the present literature review, we aim to discuss the different genetic, environmental, and microbiological causes of periodontal diseases based on evidence from the current studies in the literature. Evidence regarding genetics is still not adequate, and further research is still needed to understand the main mechanism of this etiology furtherly. Different diseases and habitual factors can contribute periodontal diseases, mainly due to increased inflammation-induced pathological events. Further attention should be directed to preventing these events to intervene against the development of periodontal diseases adequately. Early interventions against these diseases can attribute to enhance the health and prognosis of the affected patients significantly. Microbiological causes are also important and usually develop mainly as a result of poor hygiene. Therefore, further interventional research should be directed towards raising awareness among individuals to reduce the incidence of the condition.

Sex-Specific Plasticity Explains Genetic Variation in Sexual Size Dimorphism in Drosophila

The difference in body size between females and males, or sexual size dimorphism (SSD), is almost ubiquitous, and yet we have a remarkably poor understanding of the developmental-genetic mechanisms that generate it. Such an understanding is important if we are to distinguish between the many theoretical models of SSD evolution. One such model is the condition dependence hypothesis, which proposes that the body size of the larger sex is also more environmentally sensitive, a phenomenon called sex-specific plasticity (SSP). Because SSP generates differences in female and male body size, selection on plasticity may underlie the evolution of sexual size dimorphism. To test this hypothesis, however, we need to know the genetic architecture of both SSD and SSP, which is challenging because both are characteristics of populations not individuals. Here, we overcome this challenge by using isogenic lineages of Drosophila to measure both SSD and SSP for a genotype. We demonstrate extensive genetic variation for SSD among genotypes that is tightly correlated with variation in SSP, indicating that the same developmental-genetic mechanisms regulate both phenomena. These data support the condition dependence hypothesis and suggest that the observed SSD is a consequence of selection on the developmental-genetic mechanisms that regulate SSP.

A novel developmental genetic programming methodology for mathematical modeling and neuroevolution

A novel developmental genetic programming methodology for mathematical modeling and neuroevolution

A novel developmental genetic programming methodology for mathematical modeling and neuroevolution

A novel developmental genetic programming methodology for mathematical modeling and neuroevolution

DrosophilaMale Accessory Gland Displays Developmental Ground Plan of a Primitive Prostate

Conservation of developmental genetic toolkits of functionally comparable organs from disparate phyla reveals their deep homology, which may help overcome the challenges of their confounding categorization as either homologous or analogous organs. A male accessory sexual organ in mammals, prostate, for instance, is anatomically disparate from its phylogenetically distant counterpart—the male accessory gland (MAG)—in insects likeDrosophila. By examining a select set of toolkit gene expression patterns, here we show thatDrosophilaMAG displays deep homology with the mammalian prostate. Like mammalian prostate, MAG morphogenesis is marked by recruitment of fibroblast growth factor receptor, FGFR, a tubulogenesis toolkit signaling pathway, starting early during its adepithelial genesis. Specialization of the individual domains of the developing MAG tube on the other hand is marked by expression of a posterior Hox gene transcription factor, Abd-B, while Hh-Dpp signaling marks its growth.DrosophilaMAG thus reveals developmental design of unitary bud-derived tube—a ground plan that appears to have been reiteratively co-opted during evolutionary diversification of male accessory sexual organs across distant phylogeny.

The developmental genetic architecture of vocabulary skills during the first three years of life: Capturing emerging associations with later-life reading and cognition

Individual differences in early-life vocabulary measures are heritable and associated with subsequent reading and cognitive abilities, although the underlying mechanisms are little understood. Here, we (i) investigate the developmental genetic architecture of expressive and receptive vocabulary in early-life and (ii) assess timing of emerging genetic associations with mid-childhood verbal and non-verbal skills. We studied longitudinally assessed early-life vocabulary measures (15–38 months) and later-life verbal and non-verbal skills (7–8 years) in up to 6,524 unrelated children from the population-based Avon Longitudinal Study of Parents and Children (ALSPAC) cohort. We dissected the phenotypic variance of rank-transformed scores into genetic and residual components by fitting multivariate structural equation models to genome-wide genetic-relationship matrices. Our findings show that the genetic architecture of early-life vocabulary involves multiple distinct genetic factors. Two of these genetic factors are developmentally stable and also contribute to genetic variation in mid-childhood skills: One genetic factor emerging with expressive vocabulary at 24 months (path coefficient: 0.32(SE = 0.06)) was also related to later-life reading (path coefficient: 0.25(SE = 0.12)) and verbal intelligence (path coefficient: 0.42(SE = 0.13)), explaining up to 17.9% of the phenotypic variation. A second, independent genetic factor emerging with receptive vocabulary at 38 months (path coefficient: 0.15(SE = 0.07)), was more generally linked to verbal and non-verbal cognitive abilities in mid-childhood (reading path coefficient: 0.57(SE = 0.07); verbal intelligence path coefficient: 0.60(0.10); performance intelligence path coefficient: 0.50(SE = 0.08)), accounting for up to 36.1% of the phenotypic variation and the majority of genetic variance in these later-life traits (≥66.4%). Thus, the genetic foundations of mid-childhood reading and cognitive abilities are diverse. They involve at least two independent genetic factors that emerge at different developmental stages during early language development and may implicate differences in cognitive processes that are already detectable during toddlerhood.

Parallelism in Flower Evolution and Development

Flower evolution is characterized by widespread repetition, with adaptations to pollinator environment evolving in parallel. Recent studies have expanded our understanding of the developmental basis of adaptive floral novelties—petal fusion, bilateral symmetry, heterostyly, and floral dimensions. In this article, we describe patterns of trait evolution and review developmental genetic mechanisms underlying floral novelties. We discuss the diversity of mechanisms for parallel adaptation, the evidence for constraints on these mechanisms, and how constraints help explain observed macroevolutionary patterns. We describe parallel evolution resulting from similarities at multiple hierarchical levels—genetic, developmental, morphological, functional—which indicate general principles in floral evolution, including the central role of hormone signaling. An emerging pattern is mutational bias that may contribute to rapid patterns of parallel evolution, especially if the derived trait can result from simple degenerative mutations. We argue that such mutational bias may be less likely to govern the evolution of novelties patterned by complex developmental pathways.

Gene- and tissue-level interactions in normal gastrointestinal development and Hirschsprung disease

The development of the gut from endodermal tissue to an organ with multiple distinct structures and functions occurs over a prolonged time during embryonic days E10.5–E14.5 in the mouse. During this process, one major event is innervation of the gut by enteric neural crest cells (ENCCs) to establish the enteric nervous system (ENS). To understand the molecular processes underpinning gut and ENS development, we generated RNA-sequencing profiles from wild-type mouse guts at E10.5, E12.5, and E14.5 from both sexes. We also generated these profiles from homozygousRetnull embryos, a model for Hirschsprung disease (HSCR), in which the ENS is absent. These data reveal 4 major features: 1) between E10.5 and E14.5 the developmental genetic programs change from expression of major transcription factors and its modifiers to genes controlling tissue (epithelium, muscle, endothelium) specialization; 2) the major effect ofRetis not only on ENCC differentiation to enteric neurons but also on the enteric mesenchyme and epithelium; 3) a muscle genetic program exerts significant effects on ENS development; and 4) sex differences in gut development profiles are minor. The genetic programs identified, and their changes across development, suggest that both cell autonomous and nonautonomous factors, and interactions between the different developing gut tissues, are important for normal ENS development and its disorders.