Biology Open最新文献

Ocean warming is reshaping marine ecosystems and shifting species distributions. Resilient habitat-forming species help stabilize conditions for other organisms, supporting community structure under change. The tube-worm Lanice conchilega is such a habitat-former, enhancing species richness in sandy environments. Its thermal performance range remains unknown, partly because standard methods are poorly suited for this species. We present a new experimental approach to assess thermal performance based on tube-building activity, an important trait for physical protection, feeding, and habitat engineering. Spring-collected individuals were exposed in the laboratory to an ecologically relevant temperature range. Tube-building activity matched spring field conditions with a thermal minimum, optimum, and maximum at 3.6, 12.4, and 21.4°C, respectively. Performance depended strongly on recent thermal history. Because thermal tolerance can shift through acclimation, seasonal performance curves are needed to determine whether cold winters or hot summers may constrain this ecosystem engineer with potential consequences for intertidal community structure.

The 'French flag' model has long served as the prevailing framework for explaining how morphogen gradients generate spatial domains during embryonic development. However, recent evidence indicates that many tissues establish patterns by translating the sequential activation of genes into spatial domains. While the sequential nature of this process is becoming clear, the mechanisms that mediate these temporal dynamics and translate them into stable spatial boundaries remain debated. Using the gap gene network in the flour beetle Tribolium castaneum [which mediates the regionalization of the anterior-posterior (AP) axis into different axial fates through the regulation of downstream Hox genes] as a model, we combined hybridization chain reaction in situ hybridization, parental RNA interference (RNAi), and computational modeling to dissect these mechanisms. Our high-resolution spatiotemporal analysis indicates that gap genes initially function as a genetic cascade in the posterior growth zone. Specifically, RNAi perturbations reveal that the disruption of upstream genes prevents the initiation of downstream targets in the posterior rather than merely affecting their anterior maintenance. Conversely, the knockdown of downstream repressors leads to the posterior persistence of upstream genes. Furthermore, we investigated the relationship between this dynamic initiation phase and anterior maintenance. We observe that in milles-pattes (mlpt) RNAi embryos, the gap gene shavenbaby (svb) fails to propagate anteriorly out of the growth zone, indicating that the anterior maintenance of svb is actively mediated by other genes in the network. Computational simulations demonstrate that a gene network switching framework, where regulatory interactions reconfigure across the AP axis, successfully reproduces these complex phenotypes. These findings provide definitive spatiotemporal evidence that Tribolium gap gene initialization is driven by a genetic cascade, and support a model in which dynamic network rewiring converts this cascade into stable spatial patterns more anteriorly.

Mitophagy is essential for mitochondrial quality control, selectively removing damaged or superfluous mitochondria to maintain cellular health and metabolic homeostasis. While positive regulators of mitophagy are relatively well characterized, the mechanisms governing its downregulation remain less understood. In this study, we investigate the role of Saccharomyces cerevisiae Slm35 - a protein previously involved in oxidative stress response - in the regulation of mitophagy. We discovered that Slm35 is a soluble mitochondrial matrix protein and functions as a novel negative regulator of mitophagy and the mitochondrial retrograde (RTG) signaling pathway. Our results show that Slm35 modulates mitophagy through the RTG pathway, independently of Atg32 proteolytic processing by Yme1 or mitochondrial membrane potential dissipation. Notably, Slm35 is crucial for the dynamic regulation of the RTG pathway in mitophagy-inducing conditions. These findings highlight the importance of Slm35 in fine-tuning mitochondrial quality control in response to metabolic cues and suggest a critical role for dynamic RTG pathway regulation in mitophagy control.

Maintenance of proteostasis is critical for neuronal functions, as the accumulation of misfolded or damaged proteins leads to neurodegeneration. Cooling is generally neuroprotective and is used in various clinical settings. However, how it impacts neuronal proteostasis remains unclear. In rodents, the neuroprotective effects of cold have been largely attributed to the cold-inducible RNA-binding motif protein 3 (RBM3). Here, studying the human RBM3 in cultured neurons subjected to profound hypothermia, we observed its cold-induced aggregation. These RBM3 aggregates are distinct from stress granules, occur specifically in differentiated neurons, and form also at physiological temperature upon proteasomal inhibition. Thus, in humans, RBM3 aggregation may be normally counteracted by the proteasome to maintain neuronal health. Exploring the natural variation between RBM3 proteins in hibernating versus non-hibernating mammals, we discuss how the aggregation could be prevented in animals with fluctuating body temperature. These findings are important for the understanding of RBM3 functions and neuronal proteostasis and have implications for medical treatments involving incidental and induced hypothermia.

Disruptions in pancreatic development can lead to health issues such as pancreatic agenesis and congenital diabetes mellitus. Understanding pancreatic organogenesis is critical for elucidating disease mechanisms and developing regenerative therapies. The pancreas consists of endocrine and exocrine cells, both of which are derived from multipotent progenitor cells (MPCs). MPC proliferation and differentiation are tightly controlled by multiple mechanisms, including post-transcriptional regulation by miRNAs. However, these regulatory factors are not fully understood. Here, we profiled miRNA expression in MPCs and identified that mir-302 was highly enriched during the earliest stages of pancreatic development. Loss of mir-302 resulted in reduced pancreatic size without altering the proportions of endocrine and exocrine cells at E17.5, suggesting that mir-302 regulates the number of MPCs rather than their differentiation. Transcriptomic analysis at E10.5 revealed that mir-302 modulates genes associated with the Wnt signaling pathway and cell cycle progression. Notably, loss of mir-302 prolonged the S phase in MPCs, resulting in slower cell proliferation and a smaller MPC pool at E10.5. These findings provide the first comprehensive miRNA profile during early pancreatic development and establish mir-302 as a critical regulator of MPC number and pancreas size.

Melanins are the most common pigments in animals and are known to experience bleaching (molecular degradation) under UV and visible radiations. However, melanin photobleaching effects on the appearance of animals under natural sunlight conditions are unclear. Here, we collected body feathers from developing Spanish imperial eagles Aquila adalberti, mainly pigmented by the orange pheomelanin, and monitored their reflectance properties during a 15-week sunlight exposure regime. Feather brightness significantly increased with exposure time following a power function, resulting in a 1.87-times increase in paleness and an obvious loss of feather integrity. Photobleaching thus explains the gradual increase in plumage paleness exhibited by juvenile imperial eagles, changing from dark orange to yellowish during the first months of age without the course of feather molt. Bleached plumage characterizes eagle immature phenotypes until reaching a contrasting blackish phenotype by progressive molt after 5-6 years, a period during which the feather degradation that accompanies bleaching may limit flight performance. Given the pheomelanin-pigmented plumages commonly observed in juvenile raptors, and in other groups of birds in which color disappears independently of molt (e.g. wheatears, genus Oenanthe), photobleaching arises as a source of phenotypic expression that may also drive life-history strategies such as crypsis and migration.

Cohesinopathies and ciliopathies are congenital disorders affecting overlapping body systems. The extent to which these syndromes may be linked remains largely untested. Recently, reduced expression of a cohesin core subunit, Smc3, was found to result in abnormal otolith development in zebrafish embryos. This finding suggests that Smc3 may contribute to kinociliary development and function, which would represent a novel role for Smc3. Using hair cells found in neuromasts of the posterior lateral line, we found that Smc3 knockdown resulted in reduced kinociliary length. To address the role of Smc3 in kinocilial function, we monitored neomycin resistance of neuromasts (associated with several cilial gene mutants) and FM1-43X uptake in hair cells (associated with mechanotransduction). We found that Smc3 knockdown indeed led to neomycin resistance of the posterior lateral line neuromasts, suggesting impaired kinocilium function. However, neuromast hair cells did not have defects in FM1-43X uptake. We further demonstrated that hair cell number is reduced within neuromasts. This study suggests a significant influence of cohesin subunit Smc3 in ciliary structure and function and provides a preliminary link between cohesinopathy and ciliopathy etiologies.

Optimization of the soil microbiome is a promising strategy to support sustainable crop production. With the goal of developing novel bio-fertilizers for wheat cultivation, we collected fresh soil samples from ten different fields representing wheat production regions in Türkiye. Wheat seedlings (Triticum turgidum ssp. durum) were cultivated in each soil and at the three-leaf stage, DNA was isolated from the rhizospheric soil associated with each plant and the bacterial microbiome composition determined by 16S metabarcoding. Long-read sequencing was used to maximize resolution, and 1269 high-quality operational taxonomic units (OTUs) were identified. Comparisons of wheat and non-wheat rhizospheric soil identified 77 OTUs that were enriched in the wheat rhizosphere, several belonging to taxa that have previously been described as plant growth-promoting rhizobacteria. Furthermore, 209 OTUs were present in all ten wheat fields sampled, indicating that they may be ubiquitous in wheat-growing regions of Türkiye; a subset of these were also reported in wheat rhizospheric soil from other countries. Additional taxa were shown to be enriched based on local soil conditions such as pH and macronutrient content. These findings shed light onto the essential composition of the wheat rhizospheric microbiome, which provides a foundation for the development of locally adapted bio-fertilizers.

Macropinocytosis is an endocytic process that allows cells to respond to changes in their environment by internalizing nutrients and cell surface proteins, as well as modulating cell size. Here, we identify that adenosine triphosphate (ATP) triggers macropinocytosis in murine Neuro2a neuroblastoma cells, driving an increase in cell size, and internalizing the ATP release channel pannexin 1 (PANX1) to macropinosomes. Amiloride treatment and mutation of an extracellular tryptophan (W74) in PANX1 abolished ATP-evoked cell area enlargement, suggesting that PANX1 may itself regulate this form of macropinocytosis. Transient expression of the GTP-hydrolysis resistant ADP-ribosylation factor 6 GTPase (ARF6 Q67L) led to increased cell size, PANX1 internalization and localization to endosomal compartments, consistent with macropinocytosis. Inhibiting macropinocytosis-associated GTPases, phosphoinositide-3 kinase (PI3K), and disrupting actin polymerization abolished ATP-induced PANX1 internalization, supporting a macropinocytic mechanism. Further, these inhibitors disrupted co-distribution of intracellular PANX1 with macropinosomal cargo. Several lipid-PANX1 interactions were identified with relevance to macropinocytic mechanisms. The role of PANX1 in ATP-mediated macropinocytosis could be particularly important for disease states implicating PANX1, such as cancer, where ATP can act as a purinergic regulator of cell growth/metastasis and as a supplementary energy source following internalization.

Down syndrome (DS) is caused by trisomy for human chromosome 21 (Hsa21) and is associated with atypical neurodevelopment that begins prenatally. The developing human fetus receives nutritional support and gas exchange from the placenta, and normal placental function is essential for proper development. Placentas that sustain fetuses with trisomy 21 contain trisomic cells, but little is known about which Hsa21 genes are overexpressed in the placenta or their downstream molecular, cellular, and functional effects. Although access to human placentas is limited, mouse models of DS provide excellent in vivo systems for investigating the prenatal effects of trisomy. This study examined the placental transcriptome in four mouse models of DS: Dp(16)1/Yey, Ts65Dn, Ts66Yah, and Ts1Cje. Placental gene and protein expression analyses showed that trisomy increased the expression of App, Sod1, and Ifnar1 in Dp(16)1/Yey, Ts65Dn, and Ts66Yah; APP and SOD1 in Dp(16)1/Yey and Ts66Yah; and IFNAR1 in Ts66Yah. Despite modest overlap of trisomy-associated gene dysregulation among these four models, altered extracellular matrix pathways in all four models and upregulation of immune system pathways in Dp(16)1/Yey and Ts66Yah were identified. Altered redox homeostasis was observed for all four models, with Ts1Cje showing distinct changes in SOD activity and antioxidant capacity in comparison to the other three models. Immunofluorescence staining revealed region-specific upregulation of APP, SOD1, and IFNAR1 in Ts66Yah trisomic placentas. This work provides a foundation for understanding the effects of trisomy for Hsa21 orthologs on the mouse placenta and on prenatal development.