Macleanholck1390

In contrast, aggregated endodermal cells persistently lose epithelial features. These non-epithelialized aggregates, like isolated cells of all lineages, are adherent passengers for engulfment by the ectodermal epithelium. We find that collective spreading of the ectoderm and persistent de-epithelialization in the endoderm also arise during local wounding in Hydra, suggesting that Hydra's wound-healing and self-organization capabilities may employ similar mechanisms. Together, our data suggest that differing propensities for epithelialization can sort cell types into distinct compartments to build and restore complex tissue architecture.Morphological variation is the basis of natural diversity and adaptation. For example, angiosperms (flowering plants) evolved during the Cretaceous period more than 100 mya and quickly colonized terrestrial habitats [1]. A major reason for their astonishing success was the formation of fruits, which exist in a myriad of different shapes and sizes [2]. Evolution of organ shape is fueled by variation in expression patterns of regulatory genes causing changes in anisotropic cell expansion and division patterns [3-5]. However, the molecular mechanisms that alter the polarity of growth to generate novel shapes are largely unknown. The heart-shaped fruits produced by members of the Capsella genus comprise an anatomical novelty, making it particularly well suited for studies on morphological diversification [6-8]. Here, we show that post-translational modification of regulatory proteins provides a critical step in organ-shape formation. Our data reveal that the SUMO protease, HEARTBREAK (HTB), from Capsella rubella controls the activity of the key regulator of fruit development, INDEHISCENT (CrIND in C. rubella), via de-SUMOylation. click here This post-translational modification initiates a transduction pathway required to ensure precisely localized auxin biosynthesis, thereby facilitating anisotropic cell expansion to ultimately form the heart-shaped Capsella fruit. Therefore, although variation in the expression of key regulatory genes is known to be a primary driver in morphological evolution, our work demonstrates how other processes-such as post-translational modification of one such regulator-affects organ morphology.Extra-chromosomal genetic elements are important drivers of bacterial evolution, and their evolutionary success depends on positive selection for the genes they encode. Examples are plasmids encoding antibiotic resistance genes that are maintained in the presence of antibiotics (e.g., [1-3]). Plasmid maintenance is considered a metabolic burden to the host [4]; hence, when the cost of plasmid carriage outweighs its benefit, plasmid-free segregants are expected to outcompete plasmid-carrying cells, eventually leading to plasmid loss [5-7]. Thus, in the absence of positive selection, plasmid survival hinges upon stable persistence in the population. The ubiquity of plasmids in nature suggests that plasmids having a negligible effect on host fitness may evolve stable inheritance and thus gain a long-term persistence in the population, also in the absence of positive selection [8]. Nonetheless, the transition of plasmids into stably inherited genetic elements remains understudied. Here, we show that positive selection for a plasmid-encoded gene interferes with the evolution of plasmid stability. Evolving plasmids under different selection regimes in Escherichia coli, we find that antibiotics led to plasmid amplification, resulting in plasmid instability. Thus, under positive selection, suboptimal solutions for plasmid stability were maintained in the population hindering long-term plasmid persistence. Indeed, a survey of Escherichia plasmids confirms that antibiotic resistance genes are rarely found on small plasmids. Our results show that a plasmid-mediated advantage for the host may manifest in reduced plasmid evolutionary success. Considering plasmids as autonomously evolving entities holds promise for understanding the factors that govern their evolution.Communication between male and female fruit flies during courtship is essential for successful mating, but, as with many other species, it is the female who decides whether to mate. Here, we show a novel role for ovipositor extrusion in promoting male copulation attempts in virgin and mated females and signaling acceptance in virgins. We first show that ovipositor extrusion is only displayed by sexually mature females, exclusively during courtship and in response to the male song. We identified a pair of descending neurons that controls ovipositor extrusion in mated females. Genetic silencing of the descending neurons shows that ovipositor extrusion stimulates the male to attempt copulation. A detailed behavioral analysis revealed that during courtship, the male repeatedly licks the female genitalia, independently of ovipositor extrusion, and that licking an extruded ovipositor prompts a copulation attempt. However, if the ovipositor is not subsequently retracted, copulation is prevented, as it happens with mated females. In this study, we reveal a dual function of the ovipositor while its extrusion is necessary for initiating copulation by the male, its retraction signals female acceptance. We thus uncover the significance of the communication between male and female that initiates the transition from courtship to copulation.Ancient DNA has significantly improved our understanding of the evolution and population history of extinct megafauna. However, few studies have used complete ancient genomes to examine species responses to climate change prior to extinction. The woolly rhinoceros (Coelodonta antiquitatis) was a cold-adapted megaherbivore widely distributed across northern Eurasia during the Late Pleistocene and became extinct approximately 14 thousand years before present (ka BP). While humans and climate change have been proposed as potential causes of extinction [1-3], knowledge is limited on how the woolly rhinoceros was impacted by human arrival and climatic fluctuations [2]. Here, we use one complete nuclear genome and 14 mitogenomes to investigate the demographic history of woolly rhinoceros leading up to its extinction. Unlike other northern megafauna, the effective population size of woolly rhinoceros likely increased at 29.7 ka BP and subsequently remained stable until close to the species' extinction. Analysis of the nuclear genome from a ∼18.5-ka-old specimen did not indicate any increased inbreeding or reduced genetic diversity, suggesting that the population size remained steady for more than 13 ka following the arrival of humans [4]. The population contraction leading to extinction of the woolly rhinoceros may have thus been sudden and mostly driven by rapid warming in the Bølling-Allerød interstadial. Furthermore, we identify woolly rhinoceros-specific adaptations to arctic climate, similar to those of the woolly mammoth. This study highlights how species respond differently to climatic fluctuations and further illustrates the potential of palaeogenomics to study the evolutionary history of extinct species.

To determine if the size and location of facial port-wine stains (PWS) can predict glaucoma risk in neonates.

Retrospective cohort study.

Children with facial PWS who had undergone ophthalmologic examination within 4weeks of their birth were included. Clinical information, including facial photographs, intraocular pressure, corneal diameter, optic disc cup-to-disc ratio, and Sturge-Weber syndrome (SWS) diagnoses were collected. Based on facial photographs, PWS distribution, eyelid involvement, and PWS scores according to degree of involvement in each embryonic facial vasculature distribution (segment [S]1, S2 and S3) were evaluated.

Among the 34 patients, 7 (21%) had bilateral PWS lesions. Eighteen (53%) had diagnoses of glaucoma. The proportion of eyes showing PWS involving both S1 and S2 was the highest (n= 15, 37%), and the frequency of glaucoma diagnosis (n= 9, 60%) was also the greatest. In eyelid involvement analysis, among the 7 eyes with only lower-eyelid lesions, 5 (83%) had glaucoma. Among the 11 eyes with only upper-eyelid lesions, however, 2 (18%) had diagnoses of glaucoma. A logistic regression model showed that the significant factors associated with glaucoma risk were greater PWS scores in S2 (odds ratio [OR] 3.604; 95% confidence interval 1.078-12.050; P= .037) or lower-eyelid involvement (OR 12.816; 95% CI 1.698-96.744; P= .013).

Among the newborns with facial PWS, 1) a greater extent of birthmarks involving the S2 area, and 2) lesions including the lower eyelid were associated with higher risk of glaucoma development within the neonatal period.

Among the newborns with facial PWS, 1) a greater extent of birthmarks involving the S2 area, and 2) lesions including the lower eyelid were associated with higher risk of glaucoma development within the neonatal period.

To identify characteristics of loci associated with locus-level sensitivity loss or improvement during treatment with N-acetylcysteine (NAC) in retinitis pigmentosa (RP).

Retrospective analysis of prospectively collected data in the FIGHT RP clinical trial.

Patients (n= 30) were treated with 600, 1,200, or 1,800mg of NAC twice daily for 3months and then 3 times/day for 3months. Microperimetry locus-level changes between baseline and month 6 were correlated with baseline characteristics of loci using regression models. The main outcome measurement was locus-level sensitivity change ≥6 dB.

Baseline mean sensitivity (3,468 loci; 51 evaluable eyes) was 7.7 dB and for foveal, parafoveal, and perifoveal loci were 20.2, 11.8, and 5.8 dB. During treatment, 287 loci (8.28%) increased ≥6 dB, and 119 of 1,613 loci with baseline sensitivity ≥6 dB decreased ≥6 dB (7.38%). A higher dose of NAC was associated with lower likelihood of sensitivity loss ≥6 dB (P= .033). Loci with low baseline sensitivity were more likely to decrease ≥6 dB (P= .034) but also more likely to increase ≥6 dB (P < .001). Foveal versus perifoveal loci (P < .001) and superior versus inferior loci (P= .005) were more likely to increase ≥6 dB.

Higher doses of NAC reduced risk of macular loci sensitivity loss in RP. Greater sensitivity depression reversibility in the fovea during treatment suggests that high foveal cone density protects cones from irreversible loss of function in RP making them more likely to show improved function during NAC treatment.

Higher doses of NAC reduced risk of macular loci sensitivity loss in RP. Greater sensitivity depression reversibility in the fovea during treatment suggests that high foveal cone density protects cones from irreversible loss of function in RP making them more likely to show improved function during NAC treatment.

To present a novel, reproducible, and noninvasive method to quantify endothelial cell loss (ECL) of pre-stripped endothelial Descemet membrane lamellae (EDML) caused by its preparation and storage for 5days.

Prospective laboratory investigation.

Thirty EDML were stripped from corneoscleral discs and placed in a well plate containing organ culture medium 1 without dextran. An additional 5 corneoscleral discs were also placed in the same medium and served as a control group. Endothelial cell density (ECD) was measured without any additional manipulation by using spectral microscopy following an extensive protocol by which 3 clear images from the center and periphery were used for each measurement, and each measurement was repeated 5 times. ECD was measured before and directly after preparation and on days 1, 2, and 5 of storage.

The average ECD of the 30 corneoscleral discs, which later underwent stripping, was 2,292 ± 308 cells/mm

vs 2,129 ± 222 cells/mm

for the 5 corneoscleral discs of the control group.