NlOFP1 is an oviposition fluid protein deposited into rice tissue during oviposition that helps eggs resist desiccation and suppresses plant defense.

In Burkina Faso, Vitellaria paradoxa C.F. Gaertn. is one of the multipurpose species that is unfortunately attacked by numerous pests. The objective of this study is to inventory the pathogens involve...

Researchers use acoustic levitation to study midair evaporation and desiccation of COVID-19 respiratory droplets.

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AbstractTardigrades are famous for their extreme resilience, yet the role of the cytoskeleton in anhydrobiosis remains poorly understood. Here, we pharmacologically disrupted actin and microtubule networks in Paramacrobiotus gadabouti for up to 7 days prior to desiccation. Microtubule depolymerization by nocodazole or stabilization by taxol caused profound cytoskeletal changes but did not affect viability or mobility of active animals. In contrast, actin-disrupting (cytochalasin D) and actin-stabilizing (jasplakinolide) drugs induced dose-dependent mortality and severe actin network disorganization; however, many animals still survived. Strikingly, after drug washout and anhydrobiosis, nocodazole-pretreated tardigrades showed strongly reduced post-rehydration activity in a dose-dependent manner. This impairment was confirmed by automated video analysis and it correlates with extensive microtubule loss in the nervous system and sensory fields. Actin disruption altered tun morphology (producing larger, more elongated tuns) but had little effect on survival or recovery. Microtubule stabilization with taxol had no discernible behavioural effects. These findings highlight differential roles of cytoskeletal components in mechanisms of tardigrade resilience to desiccation and underscore their extraordinary tolerance to toxic compounds, allowing them to endure even severe, long-term damage to their cytoskeletal architecture.

A common theme for life across complex scales and diverse habitats and ecologies is the “fight” for survival. For some organisms, this fight will involve developing strategies that allow them to cope with conditions that hinder or limit growth, such as nutrient scarcity, extreme temperatures, desiccation, or the presence of toxic compounds. These strategies can also include escaping predators or even migrating and colonizing more suitable habitats. Becoming dormant is one strategy that allows organisms to respond to all of the above challenges (1). The definition of dormancy has varied across scientific subdisciplines and has evolved over time. In a recent opinion article on the topic, McDonald et al. (2) define dormancy as “a temporary, adaptive state of reduced metabolic activity within an extended period of arrested growth that enables a microbe to maintain viability under unfavorable environmental conditions.” This definition underlines the commitment to a specialized metabolic state that will act as a response to “wait it out,” until conditions are once more favorable for growth (3). However, given that diverse ecosystems present unique sets of challenges for survival, this behavior should be tailored to respond to specific environmental cues and is likely expressed in a wide variety of survival traits. Accordingly, dormancy can be expected to manifest differently across taxonomically and functionally distinct microbial groups.

I was just about to expire of desiccation when voila and hallelujah, the rain moved in. I am transported, relieved, overjoyed. My soul uncramps once more. Boxnoggin, however, was not nearly so pleased. We didn’t ... Read more

AbstractTardigrades are famous for their extreme resilience, yet the role of the cytoskeleton in anhydrobiosis remains poorly understood. Here, we pharmacologically disrupted actin and microtubule networks in Paramacrobiotus gadabouti for up to 7 days prior to desiccation. Microtubule depolymerization by nocodazole or stabilization by taxol caused profound cytoskeletal changes but did not affect viability or mobility of active animals. In contrast, actin-disrupting (cytochalasin D) and actin-stabilizing (jasplakinolide) drugs induced dose-dependent mortality and severe actin network disorganization; however, many animals still survived. Strikingly, after drug washout and anhydrobiosis, nocodazole-pretreated tardigrades showed strongly reduced post-rehydration activity in a dose-dependent manner. This impairment was confirmed by automated video analysis and it correlates with extensive microtubule loss in the nervous system and sensory fields. Actin disruption altered tun morphology (producing larger, more elongated tuns) but had little effect on survival or recovery. Microtubule stabilization with taxol had no discernible behavioural effects. These findings highlight differential roles of cytoskeletal components in mechanisms of tardigrade resilience to desiccation and underscore their extraordinary tolerance to toxic compounds, allowing them to endure even severe, long-term damage to their cytoskeletal architecture.

I was just about to expire of desiccation when voila and hallelujah, the rain moved in. I am transported, relieved, overjoyed. My soul uncramps once more. Boxnoggin, however, was not nearly so pleased. We didn’t ... Read more

AbstractTardigrades are famous for their extreme resilience, yet the role of the cytoskeleton in anhydrobiosis remains poorly understood. Here, we pharmacologically disrupted actin and microtubule networks in Paramacrobiotus gadabouti for up to 7 days prior to desiccation. Microtubule depolymerization by nocodazole or stabilization by taxol caused profound cytoskeletal changes but did not affect viability or mobility of active animals. In contrast, actin-disrupting (cytochalasin D) and actin-stabilizing (jasplakinolide) drugs induced dose-dependent mortality and severe actin network disorganization; however, many animals still survived. Strikingly, after drug washout and anhydrobiosis, nocodazole-pretreated tardigrades showed strongly reduced post-rehydration activity in a dose-dependent manner. This impairment was confirmed by automated video analysis and it correlates with extensive microtubule loss in the nervous system and sensory fields. Actin disruption altered tun morphology (producing larger, more elongated tuns) but had little effect on survival or recovery. Microtubule stabilization with taxol had no discernible behavioural effects. These findings highlight differential roles of cytoskeletal components in mechanisms of tardigrade resilience to desiccation and underscore their extraordinary tolerance to toxic compounds, allowing them to endure even severe, long-term damage to their cytoskeletal architecture.