Evaluating regional resiliency of coastal wetlands to sea level rise through hypsometry‐based modeling

Sea level rise (SLR) threatens coastal wetlands worldwide, yet the fate of individual wetlands will vary based on local topography, wetland morphology, sediment dynamics, hydrologic processes, and plant‐mediated feedbacks. Local variability in these factors makes it difficult to predict SLR effects across wetlands or to develop a holistic regional perspective on SLR response for a diversity of wetland types. To improve regional predictions of SLR impacts to coastal wetlands, we developed a model that addresses the scale‐dependent factors controlling SLR response and accommodates different levels of data availability. The model quantifies SLR‐driven habitat conversion within wetlands across a region by predicting changes in individual wetland hypsometry. This standardized approach can be applied to all wetlands in a region regardless of data availability, making it ideal for modeling SLR response across a range of scales. Our model was applied to 105 wetlands in southern California that spanned a broad range of typology and data availability. Our findings suggest that if wetlands are confined to their current extents, the region will lose 12% of marsh habitats (vegetated marsh and unvegetated flats) with 0.6 m of SLR (projected for 2050) and 48% with 1.7 m of SLR (projected for 2100). Habitat conversion was more drastic in wetlands with larger proportions of marsh habitats relative to subtidal habitats and occurred more rapidly in small lagoons relative to larger sites. Our assessment can inform management of coastal wetland vulnerability, improve understanding of the SLR drivers relevant to individual wetlands, and highlight significant data gaps that impede SLR response modeling across spatial scales. This approach augments regional SLR assessments by considering spatial variability in SLR response drivers, addressing data gaps, and accommodating wetland diversity, which will provide greater insights into regional SLR response that are relevant to coastal management and restoration efforts.     

Individuality in seaweeds and why we need to care

Documenting the causes and consequences of intraspecific variation forms the foundation of much of evolutionary ecology. In this Perspectives piece, we review the importance of individual variation in ecology and evolution, argue that contemporary phycology often overlooks this foundational biological unit, and highlight how this lack of attention has potentially constrained our understanding of seaweeds. We then provide some suggestions of promising but underrepresented approaches, for instance: conducting more studies and analyses at the level of the individual; designing studies to evaluate heritability and genetic regulation of traits; and measuring associations between individual variation in functional traits and ecological outcomes. We close by highlighting areas of phycological research (e.g., population biology, ecology, aquaculture, climate change management) that could benefit immediately from including a focus on individual variation. Algae, for their part, provide us with a powerful and diverse set of ecological and evolutionary traits to explore these topics. There is much to be discovered.     

Identification and expression of microRNA in the brain of hibernating bats, Myotis lucifugus

Recent research has highlighted roles for non-coding RNA i7n the regulation of stress tolerance in bats. In this study, we propose that microRNA could also play an important role in neuronal maintenance during hibernation. To explore this possibility, RT-PCR was employed to investigate the expression of eleven microRNAs from the brain tissue of euthermic control and torpid bats. Results show that eight microRNAs (miR-21, -29b, -103, -107, -124a, -132, -183 and -501) increased (1.2–1.9 fold) in torpid bats, while the protein expression of Dicer, a microRNA processing enzyme, did not significantly change during torpor. Bioinformatic analysis of the differentially expressed microRNA suggests that these microRNAs are mainly involved in two processes: (1) focal adhesion and (2) axon guidance. To determine the extent of microRNA sequence conservation in the bat, we successfully identified bat microRNA from sequence alignments against known mouse (Mus musculus) microRNA. We successfully identified 206 conserved pre-microRNA sequences, leading to the identification of 344 conserved mature microRNA sequences. Sequence homology of the identified sequences was found to be 94.76 ± 3.95% and 98.87 ± 2.24% for both pre- and mature microRNAs, respectively. Results suggest that brain function related to the differentiation of neurons and adaptive neuroprotection may be under microRNA control during bat hibernation.     

IRS1 phosphorylation does not mediate mTORC1-induced insulin resistance

Increased mammalian target of rapamycin complex 1 (mTORC1) activity has been suggested to play important roles in development of insulin resistance in obesity. mTORC1 hyperactivity also increases endoplasmic reticulum (ER) stress, which in turn contributes to development of insulin resistance and glucose intolerance. Increased IRS1 phosphorylation at Ser307 in vitro is correlated with mTORC1- and ER stress-induced insulin resistance. This phosphorylation site correlates strongly with impaired insulin receptor signaling in diabetic mice and humans. In contrast, evidence from knock-in mice suggests that phosphorylation of IRS1 at Ser307 is actually required to maintain insulin sensitivity. To study the involvement of IRS1^Ser307 phosphorylation in mTORC1-mediated glucose intolerance and insulin sensitivity in vivo, we investigated the effects of liver specific TSC1 depletion in IRS1^Ser307Ala mice and controls. Our results demonstrate that blockade of IRS1^Ser307 phosphorylation in vivo does not prevent mTORC1-mediated glucose intolerance and insulin resistance.     

Targeted Ablation of Nesprin 1 and Nesprin 2 from Murine Myocardium Results in Cardiomyopathy,Altered Nuclear Morphology and Inhibition of the Biomechanical Gene Response

Recent interest has focused on the importance of the nucleus and associated nucleoskeleton in regulating changes in cardiac gene expression in response to biomechanical load. Mutations in genes encoding proteins of the inner nuclear membrane and nucleoskeleton, which cause cardiomyopathy, also disrupt expression of a biomechanically responsive gene program. Furthermore, mutations in the outer nuclear membrane protein Nesprin 1 and 2 have been implicated in cardiomyopathy. Here, we identify for the first time a role for the outer nuclear membrane proteins, Nesprin 1 and Nesprin 2, in regulating gene expression in response to biomechanical load. Ablation of both Nesprin 1 and 2 in cardiomyocytes, but neither alone, resulted in early onset cardiomyopathy. Mutant cardiomyocytes exhibited altered nuclear positioning, shape, and chromatin positioning. Loss of Nesprin 1 or 2, or both, led to impairment of gene expression changes in response to biomechanical stimuli. These data suggest a model whereby biomechanical signals are communicated from proteins of the outer nuclear membrane, to the inner nuclear membrane and nucleoskeleton, to result in changes in gene expression required for adaptation of the cardiomyocyte to changes in biomechanical load, and give insights into etiologies underlying cardiomyopathy consequent to mutations in Nesprin 1 and 2.