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Estuaries are complex ecosystems, being difficult to determine the way management actions affect them. This study quantitatively evaluated the spread of invasive submerged and floating aquatic macrophyte vegetation in Franks Tract of the Sacramento-San Joaquin Delta in response to two types of management actions, drought salinity barriers in years 2015, 2021 and 2022, and herbicide treatments in years 2004-2022. A Random Forest algorithm applied to airborne hyperspectral and satellite multispectral images generated maps of macrophyte cover in 2004-2022. Two methods assessed the effects of the management actions. The first one compared macrophyte cover trends between Franks Tract and reference sites across the Delta. The second one predicted macrophyte cover within Franks Tract using multiple environmental variables with a Long Short-Term Memory model. According to the comparison with Big Break reference site, submerged/floating macrophyte cover was +40.9 %/+8.6 % (2015), +57.8 %/+12.7 % (2021) and +75.7 %/+34.3 % (2022) with the barrier than predicted without it. Other reference sites rendered the same tendences in 2015 but mixed results for the other years. It is questionable if these sites behave as true references. Instead, the submerged/floating macrophyte cover was +8.0 %/+0.4 % (2015), +10.3 %/-20.6 % (2021) and -22.7 %/-9.3 % (2022) with the barrier than the Long Short-Term Memory model predicted without it. Additionally, the submerged/floating macrophyte cover with the herbicide treatments was -75.8 %/-72.4 % than modeled without it throughout 2004-2022. These models would improve quantitative assessments of management effects on macrophytes with a longer time series of data that includes more periods with and without drought barriers and herbicide use., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Intercellular communication via gap junctions has a fundamental role in regulating cell growth and tissue homeostasis, and its dysregulation may be involved in cancer development and radio- and chemotherapy resistance. Connexin43 (Cx43) is the most ubiquitously expressed gap junction channel protein in human tissues. Emerging evidence indicates that dysregulation of the sorting of Cx43 to lysosomes is important in mediating the loss of Cx43-based gap junctions in cancer cells. However, the molecular basis underlying this process is currently poorly understood. Here, we identified the E3 ubiquitin ligase ITCH as a novel regulator of intercellular communication via gap junctions. We demonstrate that ITCH promotes loss of gap junctions in cervical cancer cells, which is associated with increased degradation of Cx43 in lysosomes. The data further indicate that ITCH interacts with and regulates Cx43 ubiquitination and that the ITCH-induced loss of Cx43-based gap junctions requires its catalytic HECT (homologous to E6-AP C-terminus) domain. The data also suggest that the ability of ITCH to efficiently promote loss of Cx43-based gap junctions and degradation of Cx43 depends on a functional PY (PPXY) motif in the C-terminal tail of Cx43. Together, these data provide new insights into the molecular basis underlying the degradation of Cx43 and have implications for the understanding of how intercellular communication via gap junctions is lost during cancer development., (© 2024. The Author(s).)

The inflammatory repressor TNIP1/ABIN-1 is important for keeping in check inflammatory and cell-death pathways to avoid potentially dangerous sustained activation of these pathways. We have now found that TNIP1 is rapidly degraded by selective macroautophagy/autophagy early (0-4 h) after activation of TLR3 by poly(I:C)-treatment to allow expression of pro-inflammatory genes and proteins. A few hours later (6 h), TNIP1 levels rise again to counteract sustained inflammatory signaling. TBK1-mediated phosphorylation of a TNIP1 LIR motif regulates selective autophagy of TNIP1 by stimulating interaction with Atg8-family proteins. This is a novel level of regulation of TNIP1, whose protein level is crucial for controlling inflammatory signaling.

Limitation of excessive inflammation due to selective degradation of pro-inflammatory proteins is one of the cytoprotective functions attributed to autophagy. In the current study, we highlight that selective autophagy also plays a vital role in promoting the establishment of a robust inflammatory response. Under inflammatory conditions, here TLR3-activation by poly(I:C) treatment, the inflammation repressor TNIP1 (TNFAIP3 interacting protein 1) is phosphorylated by Tank-binding kinase 1 (TBK1) activating an LIR motif that leads to the selective autophagy-dependent degradation of TNIP1, supporting the expression of pro-inflammatory genes and proteins. This selective autophagy efficiently reduces TNIP1 protein levels early (0-4 h) upon poly(I:C) treatment to allow efficient initiation of the inflammatory response. At 6 h, TNIP1 levels are restored due to increased transcription avoiding sustained inflammation. Thus, similarly as in cancer, autophagy may play a dual role in controlling inflammation depending on the exact state and timing of the inflammatory response., (© 2022 Zhou et al.)

Phenological shifts have the potential to change species interactions, but relatively few studies have used experimental manipulations to examine the effects of variation in timing of an interspecific interaction across a series of life stages of a species. Although previous experimental studies have examined the consequences of phenological timing in plant-herbivore interactions for both plants and their herbivores, less is known about their effects on subsequent plant reproduction. Here, we conducted an experiment to determine how shifts in the phenological timing of monarch (Danaus plexippus) larval herbivory affected milkweed (Asclepias fascicularis) host plant performance, including effects on growth and subsequent effects on flower and seed pod phenology and production. We found that variation in the timing of herbivory affected both plant growth and reproduction, with measurable effects several weeks to several months after herbivory ended. The timing of herbivory had qualitatively different effects on vegetative and reproductive biomass: early-season herbivory had the strongest effects on plant size, whereas late-season herbivory had the strongest effects on the production of viable seeds. These results show that phenological shifts in herbivory can have persistent and qualitatively different effects on different life stages across the season., (© 2022 The Ecological Society of America.)

NBR1 was discovered as an autophagy receptor not long after the first described vertebrate autophagy receptor p62/SQSTM1. Since then, p62 has currently been mentioned in >10,000 papers on PubMed, while NBR1 is mentioned in <350 papers. Nonetheless, evolutionary analysis reveals that NBR1, and likely also selective autophagy, was present already in the last eukaryotic common ancestor (LECA), while p62 appears first in the early Metazoan lineage. Furthermore, yeast-selective autophagy receptors Atg19 and Atg34 represent NBR1 homologs. NBR1 is the main autophagy receptor in plants that do not contain p62, while most animal taxa contain both NBR1 and p62. Mechanistic studies are starting to shed light on the collaboration between mammalian NBR1 and p62 in the autophagic degradation of protein aggregates (aggrephagy). Several domains of NBR1 are involved in cargo recognition, and the list of known substrates for NBR1-mediated selective autophagy is increasing. Lastly, roles of NBR1 in human diseases such as proteinopathies and cancer are emerging., (© 2022 Rasmussen et al.)

Gap junctions consist of arrays of intercellular channels that enable adjacent cells to communicate both electrically and metabolically. Gap junctions have a wide diversity of physiological functions, playing critical roles in both excitable and non-excitable tissues. Gap junction channels are formed by integral membrane proteins called connexins. Inherited or acquired alterations in connexins are associated with numerous diseases, including heart failure, neuropathologies, deafness, skin disorders, cataracts and cancer. Gap junctions are highly dynamic structures and by modulating the turnover rate of connexins, cells can rapidly alter the number of gap junction channels at the plasma membrane in response to extracellular or intracellular cues. Increasing evidence suggests that ubiquitination has important roles in the regulation of endoplasmic reticulum-associated degradation of connexins as well as in the modulation of gap junction endocytosis and post-endocytic sorting of connexins to lysosomes. In recent years, researchers have also started to provide insights into the physiological roles of connexin ubiquitination in specific tissue types. This review provides an overview of the advances made in understanding the roles of connexin ubiquitination in the regulation of gap junction intercellular communication and discusses the emerging physiological and pathophysiological implications of these processes.

Intercellular communication via gap junctions has an important role in controlling cell growth and in maintaining tissue homeostasis. Connexin 43 (Cx43; also known as GJA1) is the most abundantly expressed gap junction channel protein in humans and acts as a tumor suppressor in multiple tissue types. Cx43 is often dysregulated at the post-translational level during cancer development, resulting in loss of gap junctions. However, the molecular basis underlying the aberrant regulation of Cx43 in cancer cells has remained elusive. Here, we demonstrate that the oncogenic E3 ubiquitin ligase NEDD4 regulates the Cx43 protein level in HeLa cells, both under basal conditions and in response to protein kinase C activation. Furthermore, overexpression of NEDD4, but not a catalytically inactive form of NEDD4, was found to result in nearly complete loss of gap junctions and increased lysosomal degradation of Cx43 in both HeLa and C33A cervical carcinoma cells. Collectively, the data provide new insights into the molecular basis underlying the regulation of gap junction size and represent the first evidence that an oncogenic E3 ubiquitin ligase promotes loss of gap junctions and Cx43 degradation in human carcinoma cells., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2017. Published by The Company of Biologists Ltd.)

Timing of phenological events varies among years with natural variation in environmental conditions and is also shifting in response to climate change. These phenological shifts likely have many effects on species interactions. Most research on the ecological consequences of phenological shifts has focused on variation in simple metrics such as phenological firsts. However, for a population, a phenological event exhibits a temporal distribution with many attributes that can vary (e.g., mean, variance, skewness), each of which likely has distinct effects on interactions. In this study, we manipulated two attributes of the phenological distribution of a prey species to determine their individual and combined effects on predator-prey interactions. Specifically, we studied how shifts in the mean and variation around the mean (i.e., synchrony) of hatching by tadpoles (Hyla cinerea) affected interactions with predatory dragonfly naiads (Tramea carolina). At the end of larval development, we quantified survival and growth of predator and prey. We found that both types of shifts altered demographic rates of the prey; that the effects of synchrony shifts, though rarely studied, were at least as strong as those due to mean shifts; and that the combined effects of shifts in synchrony and mean were additive rather than synergistic. By dissecting the roles of two types of shifts, this study represents a significant step toward a comprehensive understanding of the complex effects of phenological shifts on species interactions. Embracing this complexity is critical for predicting how climate change will alter community dynamics., (© 2016 by the Ecological Society of America.)

Based on trends in medical education and in patient management we discuss how new hospitals can be designed to focus on healthcare education. Hospitals have a major commitment and responsibility in the education of all kinds of undergraduate and postgraduate healthcare professionals, and this calls for dedicated environments. New hospitals must be designed not only for patient management, but also for healthcare education. This article is written by a multidisciplinary group and includes experiences within hospital management, medical education, implementation and architecture.

Phenology is increasingly recognized as an important factor structuring communities because it determines when and at what life stage organisms interact. Previous work indicates that changes in first or mean timing of a phenological event can affect populations and communities, but little is known about the consequences of changes in the distribution (e.g., synchrony) of a phenological event. We conducted an experiment using an anuran study system to determine how synchrony of reproduction and egg hatching affects offspring performance, whether the effects are density dependent, and how hatching synchrony influences the synchrony of a subsequent phenological event (metamorphosis). Changes in hatching synchrony altered survival, development rates, and body size at metamorphosis, which can affect post-metamorphosis performance. The degree of synchrony at hatching also affected the degree of synchrony at metamorphosis, indicating that timing of one stage can carry over to affect that of later ones. Importantly, these effects were all density dependent, likely because decreasing hatching synchrony switched intraspecific interactions from scramble to contest competition. This study demonstrates that phenological synchrony has important consequences for ecological interactions and population dynamics, emphasizing the need to develop a comprehensive understanding of how shifts in phenological distributions affect communities.