When mother knows best: A population genetic model of transgenerational versus intragenerational plasticity

Many organisms exhibit phenotypic plasticity; producing alternate phenotypes depending on the environment. Individuals can be plastic (intragenerational or direct plasticity), wherein individuals of the same genotype produce different phenotypes in response to the environments they experience. Alternatively, an individual's phenotype may be under the control of its parents, usually the mother (transgenerational or indirect plasticity), so that mother's genotype determines the phenotype produced by a given genotype of her offspring. Under what conditions does plasticity evolve to have intragenerational as opposed to transgenerational genetic control? To explore this question, we present a population genetic model for the evolution of transgenerational and intragenerational plasticity. We hypothesize that the capacity for plasticity incurs a fitness cost, which is borne either by the individual developing the plastic phenotype or by its mother. We also hypothesize that individuals are imperfect predictors of future environments and their capacity for plasticity can lead them occasionally to make a low‐fitness phenotype for a particular environment. When the cost, benefit and error parameters are equal, we show that there is no evolutionary advantage to intragenerational over transgenerational plasticity, although the rate of evolution of transgenerational plasticity is half the rate for intragenerational plasticity, as predicted by theory on indirect genetic effects. We find that transgenerational plasticity evolves when mothers are better predictors of future environments than offspring or when the fitness cost of the capacity for plasticity is more readily borne by a mother than by her developing offspring. We discuss different natural systems with either direct intragenerational plasticity or indirect transgenerational plasticity and find a pattern qualitatively in accord with the predictions of our model.     

Maternal and larval niche construction interact to shape development,survival, and population divergence in the dung beetle Onthophagus taurus

Through niche construction, organisms modify their environments in ways that can alter how selection acts on themselves and their offspring. However, the role of niche construction in shaping developmental and evolutionary trajectories, and its importance for population divergences and local adaptation, remains largely unclear. In this study, we manipulated both maternal and larval niche construction and measured the effects on fitness‐relevant traits in two rapidly diverging populations of the bull‐headed dung beetle, Onthophagus taurus. We find that both types of niche construction enhance adult size, peak larval mass, and pupal mass, which when compromised lead to a synergistic decrease in survival. Furthermore, for one measure, duration of larval development, we find that the two populations have diverged in their reliance on niche construction: larval niche construction appears to buffer against compromised maternal niche construction only in beetles from Western Australia, but not in beetles from the Eastern United States. We discuss our results in the context of rapid adaptation to novel conditions and the role of niche construction therein.     

Skin Filling and Firming Activity of a Hyaluronic Acid Inducing Synthetic Tripeptide

International Journal of Peptide Research and Therapeutics - Aging of skin manifests in loss of volume and firming due to degradation of extracellular matrix components such as collagen and...     

Characteristics and management of congenital esophageal stenosis: findings from a multicenter study

Background

Congenital esophageal stenosis (CES) is a rare condition frequently associated with esophageal atresia (EA). There are limited data from small series about the presentation, treatment, and outcomes of CES.

Methods

Medical records of all patients with CES included in the French Network on Esophageal Malformations and Congenital Diseases were reviewed retrospectively with regard to diagnosis, treatment, and outcome.

Results

Over 18 years, 61 patients (30 boys) had CES, and 29 (47%) of these patients also had EA. The mean age at diagnosis was 24 months (1 day to 14 years) and was younger in patients with CES and EA than in those with isolated CES (7 vs. 126 months, p?<?0.05). Twenty-one of the 61 patients with CES had no clinical symptoms: in three patients, the findings were incidental, and in 18 of the 29 patients with associated EA, CES was diagnosed at the time of surgical repair of EA or during a postoperative systematic esophageal barium study. In the 40 other patients, at diagnosis, 50% presented with dysphasia, 40% with vomiting, 50% with food impaction, and 42% with respiratory symptoms. Diagnosis of CES was confirmed by esophageal barium study (56/61) and/or esophageal endoscopy (50/61). Sixteen patients had tracheobronchial remnants (TBR), 40 had fibromuscular stenosis (FMS), and five had membrane stenosis (MS). Thirty-four patients (56%) were treated by dilation only (13/34 remained asymptomatic at follow-up); 15 patients were treated by dilation but required later surgery because of failure (4/15 remained asymptomatic at follow-up); and nine patients had a primary surgical intervention (4/9 were asymptomatic at follow-up). Dilation was complicated by esophageal perforation in two patients (3.4%). At follow-up, dysphagia remained in 36% (21/58) of patients, but the incidence did not differ between the EA and the isolated CS groups (10/29 vs. 7/32, p?=?0.27).

Conclusions

CS diagnosis can be delayed when associated with EA. Dilation may be effective for treating patients with FMS and MS, but surgical repair is often required for those with TBR. Our results show clearly that, regardless of the therapeutic option, dysphagia occurs frequently, and patients with CES should be followed over the long term.

     

Therapeutic antibodies and infectious diseases,Tours, France,November 20−22, 2012

The Therapeutic Antibodies and Infectious Diseases international congress was held in Tours, France on November 20−22, 2012. The first session was devoted to the development of antibodies directed against bacterial toxins or viruses that could be used in a potential bioterrorist threat situation. The second session dealt with the effector functions of anti-microbial antibodies, while the third was oriented toward anti-viral antibodies, with a special emphasis on antibodies directed against the human immunodeficiency and hepatitis C viruses. After a lecture by a speaker from the US Food and Drug Administration on antibody cocktails, the second day ended with a special session dedicated to discussions regarding the involvement of French biotechnology industries in the field. On the last day, the congress concluded with talks about current antibody treatments for infectious diseases, with a particular focus on their adverse events. Participants enjoyed this very stimulating and convivial meeting, which gathered scientists from various countries who had different scientific research interests.     

Tcf15 Primes Pluripotent Cells for Differentiation

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Highlights? Tcf15 marks a subpopulation of pluripotent cells primed for somatic lineages ? Tcf15 expression is regulated by FGF signaling ? Tcf15 activity is repressed by Id proteins ? Tcf15 represses Nanog and drives differentiation once released from Id inhibition     

PMEL: a pigment cell‐specific model for functional amyloid formation

PMEL is a pigment cell‐specific protein responsible for the formation of fibrillar sheets within the pigment organelle, the melanosome. The fibrillar sheets serve as a template upon which melanins polymerize as they are synthesized. The PMEL fibrils are required for optimal pigment cell function, as animals that either lack PMEL expression or express mutant PMEL variants show varying degrees of hypopigmentation and pigment cell inviability. The PMEL fibrils have biophysical properties of amyloid, a protein fold that is frequently associated with neurodegenerative and other diseases. However, PMEL is one of a growing number of non‐pathogenic amyloid proteins that contribute to the function of the cell and/or organism that produces them. Understanding how PMEL generates amyloid in a non‐pathogenic manner might provide insights into how to avoid toxicity due to pathological amyloid formation. In this review, we summarize and reconcile data concerning the fate of PMEL from its site of synthesis in the endoplasmic reticulum to newly formed melanosomes and the role of distinct PMEL subdomains in trafficking and amyloid fibril formation. We then discuss how its progression through the secretory pathway into the endosomal system might allow for the regulated and non‐toxic conversion of PMEL into an ordered amyloid polymer.