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Biology subjects

Herrera, E.

Publications and source records attributed to Herrera, E..

8 recordsLinked to original sources

Soil microbial diversity alters soil microhydrology through extracellular polymeric substance production

Soil microbial communities have a variety of mechanisms to deal with emerging drought stress. One well-documented mechanism is increased microbial production of extracellular polymeric substances (EPS), which can potentially change the soil density and water holding capacity. Yet little is known about how microbial diversity influences the functional capacity of EPS formation and the resulting outcomes in water dynamics. To understand more about communal microbiome EPS production, we set up sterile mesocosms where we examined the effects of microbial diversity (high or low treatments) and nutrient input (supplement or deficient treatments) on these processes. To capture the microhydrology of the mesocosms, we measured water holding (WH), infiltration, evaporation, and soil properties we believe microbes are altering (EPS, soil aggregation). Our hypothesis stated that if diversity was artificially manipulated, then soil-water properties will be altered via production of EPS. We predicted that low diversity systems would have lower functional diversity, leading to less EPS production, moisture storage, and minimal changes from inert soil media. As predicted, we found that the high-diversity systems had a higher water retention and lower rates of water loss over time than low-diversity systems. This trend was magnified in the nutrient-supplemented treatment, suggesting that EPS production and subsequent water-holding traits are emergent features of the microbiome. Unexpectedly, we observed a correlation between the amount of water retained and the quantity of lipid EPS produced. This suggests that EPS composition, rather than quantity, is determinative of a biofilms function. In conclusion, it appears that microbial diversity influences soil properties that are important to moisture retention within these systems. To date, the role that microbes and their diversity play in soil hydrology has been severely understudied, so this work aims to build ecological understandings of these systems. These findings are valuable, for if we learn how microbes manipulate soil moisture, we can apply these functions to advance sustainable agricultural practices and enhance ecosystem resilience to water scarcity in arid regions. Open Research StatementUpon publication data, and code will be made available through Zenodo. Sequencing data will be uploaded to NCBI SRA.

ecology↗

ARID1A-BAF coordinates ZIC2 genomic occupancy for epithelial to mesenchymal transition in cranial neural crest lineage commitment

The BAF chromatin remodeler regulates lineage commitment including cranial neural crest cell (CNCC) specification. Variants in BAF subunits cause Coffin-Siris Syndrome (CSS), a congenital disorder characterized by coarse craniofacial features and intellectual disability. Approximately 50% of CSS patients carry variants in one of the mutually exclusive BAF subunits, ARID1A/ARID1B. While Arid1a deletion in mouse neural crest causes severe craniofacial phenotypes, little is known about the role of ARID1A in CNCC specification. Using CSS patient-derived ARID1A+/- iPSCs to model CNCC specification, we discovered ARID1A-haploinsufficiency impairs epithelial to mesenchymal transition (EMT), a process necessary for CNCC delamination and migration from the neural tube. Furthermore, wild-type ARID1A-BAF regulates enhancers associated with EMT genes. ARID1A-BAF binding at these enhancers is impaired in heterozygotes while binding at promoters is unaffected. At the sequence level, these EMT enhancers contain binding motifs for ZIC2, and ZIC2 binding at these sites is ARID1A-dependent. When excluded from EMT enhancers, ZIC2 relocates to neuronal enhancers, triggering aberrant neuronal gene activation. In mice, deletion of Zic2 impairs NCC delamination, while ZIC2 overexpression in chick embryos at pre-migratory neural crest stages elicits ectopic delamination from the neural tube. These findings reveal a novel ARID1A-ZIC2 axis essential for EMT and CNCC delamination.

developmental biology↗

Obesogenic diet in mice leads to inflammation and oxidative stress in the mother in association with sex-specific changes in fetal development, inflammatory markers and placental transcriptome

IntroductionObesity during pregnancy is related to adverse maternal and neonatal outcomes. Factors involved in these outcomes may include increased maternal insulin resistance, inflammation, oxidative stress and nutrient mishandling. The placenta is the primary determinant of fetal outcomes, and its function can be impacted by maternal obesity. The aim of this study in mice was to determine the effect of obesity on maternal lipid handling, inflammatory and redox state, and placental oxidative stress, inflammatory signaling, and gene expression relative to female and male fetal growth. MethodsFemale mice were fed control or obesogenic high-fat/high-sugar diet (HFHS) from 9 weeks prior to and during pregnancy. On day 18.5 of pregnancy, maternal plasma, and liver, placenta, and fetal serum were collected to examine the immune and redox state. The placental labyrinth zone (Lz) was dissected for RNA-sequencing analysis of gene expression changes. ResultsHFHS diet induced, in the dams, hepatic steatosis, oxidative stress (reduced catalase, elevated protein oxidation) and activation of pro-inflammatory pathways (p38-MAPK) along with imbalanced circulating cytokine concentrations (increased IL-6 and decreased IL-5 and IL-17A). HFHS fetuses were asymmetrically growth-restricted, showing sex-specific changes in circulating cytokines (GM-CSF, TNF-, IL-6 and IFN-{gamma}). Morphology of the placenta Lz was modified by a HFHS diet, in association with sex-specific alterations in the expression of genes and proteins implicated in oxidative stress, inflammation, and stress signaling. Placental gene expression changes were comparable to that seen in models of intrauterine inflammation and were related to a transcriptional network involving transcription factors, LYL1 and PLAG1. DiscussionThis study shows that fetal growth restriction with maternal obesity is related to elevated oxidative stress, inflammatory pathways, and sex-specific placental changes. Our data are important given the marked consequences and the rising rates of obesity worldwide.

physiology↗

A novel regulatory mechanism of actin cytoskeleton dynamics through a neural microexon in DAAM1 is necessary for memory formation

Actin cytoskeleton dynamics is critical for nervous system development and function, yet the role of alternative splicing in controlling these processes is poorly understood. A highly conserved subset of neuronal-specific microexons coordinates fundamental aspects of nervous system biology. A subset of these exons is enriched in genes involved in actin cytoskeleton, yet their functions are unknown. Here, we focus on a microexon in DAAM1, a member of the formin-homology-2 (FH2) domain class of proteins, which have diverse functions associated with the reorganization of the actin cytoskeleton. Remarkably, splicing of the microexon extends the linker region of the DAAM1 FH2 domain and leads to qualitative and quantitative changes in actin polymerization. Deletion of the microexon results in neuritogenesis defects and increased calcium influx in differentiated neurons. Moreover, mice harboring the deletion exhibit postsynaptic defects, reduced number of immature dendritic spines, impaired long-term potentiation, and deficits in memory formation. These deficits are associated with increased RHOA/ROCK signaling, pivotal in controlling actin-cytoskeleton dynamics, and were rescued by treatment with a ROCK inhibitor. We thus demonstrate that a conserved neuronal microexon in DAAM1 is critical for controlling actin dynamics through the RHOA/ROCK signaling pathway and is necessary for normal cognitive functioning.

neuroscience↗

Perinatal correlated retinal activity is required for the wiring of visual axons in non-image forming nuclei

The development of the visual system is an intricate and multi-step process involving the precise connection of retinal ganglion cell (RGC) axon terminals with their corresponding neurons in the visual nuclei of the brain. Upon reaching primary image-forming nuclei (IFN), such as the superior colliculus and the lateral geniculate nucleus, RGC axons undergo extensive arborization that refines over the first few postnatal weeks. The molecular mechanisms driving this activity-dependent remodeling process, which is influenced by spontaneous activity in the developing retina, are still not well understood. In this study, by manipulating the activity of RGCs in mice and analyzing their transcriptomic profiles before eye opening, we have identified gene programs involved in activity-dependent refinement. Furthermore, while RGC axons also target non-image forming nuclei (NIFN), the impact of spontaneous retinal activity on the development of these accessory nuclei, has not yet been elucidated. The analysis of visual terminals from mice with altered retinal activity revealed that spontaneous retinal waves occurring prior to visual experience also play a role in shaping the connectivity of the non-image forming circuit. Overall, these findings contribute to a deeper understanding of the mechanisms governing activity-dependent axon refinement during the establishment of the visual circuit.

neuroscience↗

CyclinD2-mediated regulation of neurogenic output from the retinal ciliary margin is perturbed in albinism

In albinism, aberrations in the ipsi-/contralateral retinal ganglion cell (RGC) ratio compromise the functional integrity of the binocular circuit. We focus here on the mouse ciliary margin zone (CMZ), a neurogenic niche at the embryonic peripheral retina, to investigate developmental processes regulating RGC neurogenesis and identity acquisition. We found that the mouse ventral CMZ has the competence to generate predominantly ipsilaterally-projecting RGCs, but this competence is altered in the albino visual system due to CyclinD2 downregulation and disturbed temporal control of the cell cycle. Consequently, albino as well as CyclinD2-deficient pigmented mice exhibit a diminished ipsilateral retinogeniculate projection and compromised depth perception. Pharmacological stimulation of calcium channels in albino mice, known to upregulate CyclinD2 in other cell types, augmented CyclinD2-dependent neurogenesis of ipsilateral RGCs, and improved stereopsis. Together, these results implicate CMZ neurogenesis and its regulators as critical for the formation and function of the mammalian binocular circuit. HighlightsO_LIThe mouse ventral CMZ produces predominantly ipsilateral RGCs. C_LIO_LIIn the albino visual system, CyclinD2 downregulation leads to delayed G1/S transition toward mitotic exit of CMZ progenitors. C_LIO_LIPerturbations in the temporal control of cell cycle by CyclinD2 lead to reduced Zic2+ RGCs and consequently, a diminished ipsilateral retinogeniculate projection and compromised depth perception. C_LIO_LICalcium channel modulation during embryogenesis normalizes the levels of CyclinD2 and restores binocular vision in albino mice. C_LI

developmental biology↗

A first assessment of the distribution and abundance of large pelagic species at Cocos Ridge seamounts (Eastern Tropical Pacific) using drifting pelagic baited remote cameras

Understanding the link between seamounts and large pelagic species (LPS) is critical for guiding management and conservation efforts in open water ecosystems. The seamounts along the Cocos Ridge in the Eastern Tropical Pacific (ETP) are thought to play a critical role for LPS moving between Cocos Island (Costa Rica) and Galapagos Islands (Ecuador). However, to date, research efforts to understand pelagic community structure beyond the borders of these oceanic Marine Protected Areas (MPAs) have been limited. This study used drifting-pelagic baited remote underwater video stations (BRUVS) to characterize the distribution and relative abundance of LPS at Cocos Ridge seamounts. Our drifting-pelagic BRUVS detected a total of 21 species including sharks, large teleosts, small teleosts, dolphins and one sea turtle, of which 4 are threatened species. Relative abundance and richness of LPS was significantly higher at shallow seamounts (<400m) compared to deeper ones (>400m) suggesting that seamount depth could be an important driver structuring LPS assemblages along the Cocos Ridge. Our cameras provided the first visual evidence of the schooling behaviour of S. lewini at two shallow seamounts outside the protection limits of Cocos and Galapagos Islands. However, further research is still needed to demonstrate a positive association between LPS and Cocos Ridge seamounts. Our findings showed that drifting pelagic BRUVS are an effective tool to survey LPS in fully pelagic ecosystems of the ETP. This study represents the first step towards the standardization of this technique throughout the region.

ecology↗

Zic2 abrogates an alternative Wnt signaling pathway to convert axon attraction into repulsion

Wnt signaling is involved in axon pathfinding during brain wiring but it is unknown how Wnt ligands promote attraction or repulsion. In addition, the participation of the canonical ({beta}catenin-dependent transcription) versus non-canonical ({beta}catenin-independent) Wnt pathways in this process remains controversial. Here we show that Wnt5a is expressed at the optic chiasm midline and promotes axon crossing by triggering an alternative Wnt pathway that depends on polarized accumulation of {beta}catenin at the axon terminal but does not activate the canonical pathway. Remarkably, this alternative pathway is silenced by the transcription factor Zic2 in the small subset of ipsilaterally projecting neurons. Zic2 directly regulates genes related to Wnt and Eph signaling that lead to global accumulation of {beta}catenin but triggers its asymmetric phosphorylation to facilitate the steering of the growth cone. This alternative Wnt pathway found in contralateral axons and its Zic2-mediated abrogation in ipsilateral neurons is likely operating in many other contexts requiring a two-way response to Wnt ligands.

developmental biology↗