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Parada, C.

Publications and source records attributed to Parada, C..

3 recordsLinked to original sources

Disruption of hemocyte differentiation and distribution in Drosophila Ptr23c mutants

In Drosophila, hemocytes are essential for development and immunity, with their differentiation and spatial distribution under strict regulation. Here, we examine the effect of the Ptr23c null mutation in embryonic hemocyte development. Contrary to our initial hypothesis, Ptr does not regulate hemocyte number, as the mutation did not affect the total number of hemocytes, apoptosis, mitosis, or the balance between major subpopulations. However, Ptr23c mutants displayed disrupted distribution and premature hemocyte differentiation, marked by accelerated maturation at stage 12. Despite this early differentiation, Ptr23c embryos exhibited a 50% reduction in mature hemocytes by stage 16, as quantified by serpent-driven mCherry expression. Our findings establish Ptr as a regulator of hemocyte distribution and differentiation timing during normal embryogenesis, possibly through modulation of the serpent pathway.

developmental biology↗

Survival, Movement, and Lifespan: Decoding the Roles of Patched-Related (Ptr) in Drosophila melanogaster

Patched-related (Ptr) is a transmembrane protein implicated in developmental processes in Drosophila melanogaster, yet its precise role remains incompletely understood. Here, we use Ptr23c null mutants to investigate the functional significance of Ptr through the entire life cycle monitoring survival during embryonic, larval, pupal and adult development, and studying larval locomotion and muscle structure. We report that Ptr23c larvae displayed impaired hatching, indicative of defective embryonic development. Moreover, mutant larvae exhibited reduced mobility and lethargy, suggesting a potential involvement of Ptr in neuromuscular function. Morphological analysis of somatic muscles in mutant larvae revealed enlarged cell nuclei. Despite high pre-adult mortality, a subset of Ptr23c mutant adults display an unexpected extension in lifespan compared to controls, implicating Ptr in the regulation of longevity. Our findings provide critical insights into the multifaceted role of Ptr in Drosophila development, highlighting its contributions to post-embryonic survival, neuromuscular function, and lifespan regulation. This study underscores the significance of exploring broader genetic networks to unravel the complexities of developmental processes. Highlights- Loss of Ptr elicits impaired embryonic hatching, reduced mobility, and lethargy. - Ptr23c mutants display nuclear enlargement in somatic muscles. - Ptr23c individuals that survive to adulthood demonstrate extended longevity.

developmental biology↗

Growth-dependent concentration gradient of the oscillating Min system in Escherichia coli

The Min system contributes to the spatiotemporal regulation of division sites in Escherichia coli. The MinD and MinE proteins of this system self-organize into oscillatory waves in the form of concentration gradients. How the intracellular Min protein concentration gradients are coordinated with cell growth to achieve spatiotemporal accuracy of cell division is unknown. Here, we report that the MinD concentration gradient becomes progressively steeper as cells elongate, suggesting that the division inhibitory activity at the midcell also decreases with cell growth. Interestingly, the oscillation period appears relatively stable across different cell lengths. Similar features were found in cells under carbon stress conditions, but the gradient was even steeper, likely favoring division at shorter cell lengths. The length-dependent variation of the concentration gradient was further examined in silico using a reaction-diffusion model, which not only supported the above features, but also revealed a decrease in the midcell concentration as the shape of the gradient becomes steeper in growing cells. This growth-dependent regulation of the midcell concentration of MinD may be coupled with the FtsZ ring formation through the MinD-interacting protein MinC. We found that the variable concentration gradients occur by coordinating the reaction rates of the recruitment of MinD and MinE to the membrane and the recharging of MinD with ATP in the cytoplasm. In conclusion, this work uncovers the plasticity of MinD concentration gradients during interpolar oscillations throughout cell growth, an intrinsic property integrated during cell division.

cell biology↗