לוח שנה משולב

Subsurface systems, such as alluvial aquifers and soils, store and govern the quality of groundwater by sustaining a unique balance of biogeochemical and hydrological processes. The complex characteristics of subsurface systems are demonstrated in both spatial and compositional sediment heterogeneities that ultimately control the rate and extent of elemental cycling. Different redox environments commonly form within the subsurface and may largely influence these cycles. Heavy metals, occurring naturally (geogenic) or as anthropogenic contaminants, are particularly sensitive to varying redox conditions, even if they are not directly redox active.
In this seminar, I will show how sediment hotspots and interfaces influence elemental cycling, contaminant attenuation, and groundwater quality. I will present examples of how an alluvial aquifer system exhibiting redox heterogeneities may influence heavy metal mobility by preferential retention in fine-grained sediment lenses embedded within the coarse aquifer. Several mechanisms contribute to the retention in fine-grained sediments, and we also observe a significant impact of nitrate-rich conditions on the extent and phases of metal retention.
Further, I will share our findings on the dynamic and unique composition of iron-rich colloids, detected in reducing zones of a floodplain subsurface. Our results demonstrate the presence of partially oxidized iron rich colloids in otherwise reducing conditions, thanks to a protective organic-silicon coating. The lifecycle and composition of these colloids may have direct effects on element cycling as they may serve as vectors for the transport of nutrients and organic matter into groundwater and surface water recipients.
Lastly, I will present my future research visions, in a lab devoted to the study of biogeochemical heterogeneity and coupled elemental cycling under dynamic conditions.

Biological systems sense and respond to mechanical forces. The hallmark of a mechano-sensing molecule is a functional switch when subjected to a mechanical force. I will present results on how we have identified, using Molecular Dynamics simulations in conjunction with biophysical experiments, protein molecules and protein-based materials as new candidates for such mechanical switches. These include kinases such as Focal Adhesion Kinase and Src kinase. I will also show how we discovered collagen upon tension to generate mechanoradicals and oxidative stress molecules through scission of chemical bonds. As a source and buffer of oxidative signaling molecules, collagen is not a mere force-carrying material but instead can forward mechanical stimuli to biochemical circuits.

Most of the Pacific Northwest (PNW, USA) and British Columbia
experienced extraordinarily high air temperatures during an extreme heat
wave event (“heat dome”) in late June of 2021. In many locations, alltime
record high air temperatures (Tair) exceeding 40-45 °C were
observed. In this talk I will present evidence of the widespread impacts of
this extreme heat event. These impacts include foliar damage observed in
many locations of this region, along with some tree mortality.
Additionally, I will present data from dendrometers and eddy covariance
towers in contrasting forest types highlighting the impacts on tree growth
and ecosystem-atmosphere CO2, H2O, and energy fluxes. Better
understanding the environmental drivers, biophysical and physiological
mechanisms, and ecological consequences of heat damage incurred by
forests is of broad relevance and societal importance.

The mitoribosome translates specific mitochondrial mRNAs and regulates energy production that is a signature of all eukaryotic life forms. We present cryo-EM analyses of its assembly intermediates, mRNA binding process, and nascent polypeptide delivery to the membrane. To study the assembly mechanism, we determined a series of the small mitoribosomal subunit intermediates in complex with auxiliary factors that explain how action of step-specific factors establishes the catalytic mitoribosome. Its activation is then performed by LRPPRC that forms a stable complex with SLIRP, which delivers mRNA to the mitoribosome. In mammals, LRPPRC stabilised mRNAs co-transcriptionally, thus it links the entire gene expression system. Specific mitoribosomal proteins align the delivered mRNA with tRNA in the decoding center. This allows a nascent polypeptide to form in the tunnel, and next it needs to be delivered to the mitochondrial inner membrane. Here, we report the human mitoribosomes bound to the insertase OXA1, which elucidates the basis by which protein synthesis is coupled to membrane delivery. Finally, comparative structural and biochemical analyses reveal functionally important binding of cofactors NAD, ATP, GDP, iron-sulfur clusters and polyamines. Together with experimental identification of specific rRNA and protein modifications, the data illuminate principal components responsible for the translation of genetic material in mitochondria.

For decades, Alzheimer's disease (AD) was perceived as a disease of the neuron alone. However, research advances in recent years have challenged this concept and shed light on the critical roles of other cells within the central nervous system (CNS) and the periphery. Within the CNS, microglia and astrocytes were revealed to be key players in disease progression, while other cell types, such as oligodendrocytes, pericytes, and endothelial cells, remained relatively understudied. In my PhD, I focused on understanding how two non-neuronal cell types, the oligodendroglia in the brain parenchyma and the choroid plexus (CP) epithelium, respond to AD and how they possibly affect pathological processes. My research identified a cellular state of oligodendrocytes that significantly increased in association with brain pathology, which we termed disease-associated oligodendrocytes (DOLs). Oligodendrocytes with DOL signature could also be identified in a mouse model of tauopathy and other neurodegenerative and autoimmune inflammatory conditions, suggesting a common response of oligodendrocytes to severe deviation from homeostasis. In the second part of my PhD, I contributed to a research aiming to investigate the mechanisms underlying the decline of the CP's neuroprotective abilities in the context of AD. We found that exposure of choroid plexus epithelial cultures to 24-hydroxycholesterol (24-OH), the enzymatic product of the brain-specific enzyme cholesterol 24-hydroxylase (CYP46A1), results in downregulation of aging- related transcriptomic signatures-such as Interferon type I (IFN-I) associated inflammation. Moreover, we found that CYP46A1 is constitutively expressed by the CP of humans and mice but is reduced in AD patients and 5xFAD mice. Overexpression of Cyp46a1 at the CP in 5xFAD mice attenuated cognitive loss and brain inflammation. Our results suggest that CP CYP46A1 is an unexpected safeguard against chronic anti-viral-like responses that can be rescued when lost. Overall, my PhD work highlights the significance of studying the fate of non-neuronal cell types in neurodegenerative diseases, in general, and in AD, in particular, and emphasizes the potential of next- generation transcriptomic techniques as a powerful tool to unveil previously unexpected pathways and mechanisms involved in these diseases. 
Zoom link-https://weizmann.zoom.us/j/98815291638?pwd=cnZTanhzWkEyYmh4Mjk4OWxHMGE5UT09
Meeting ID:988 1529 1638
Password:880170