Biology subjects

Lee, M.-J.

Publications and source records attributed to Lee, M.-J..

3 recordsLinked to original sources

bioRxiv2025

Rigid Control of Motor Unit Firing Rates in the Human Tibialis Anterior Muscle Persists during Neurofeedback

The conventional framework of motor-unit (MU) control assumes that MUs in a MU pool are constrained by a fixed recruitment order and a common input. This rigid-control framework has been challenged by recent findings suggesting that MU activity could be flexibly modulated, potentially mediated by descending cortical inputs. In this study, rather than evaluating flexibility from the perspective of recruitment thresholds, we investigated control flexibility by assessing if human participants can voluntarily modulate MU firing rates beyond rigid-control constraints. Specifically, we examined whether participants could voluntarily modulate the firing rates of a pair of MUs from the tibialis anterior muscle during real-time feedback. Two tasks involving target-reach with different visual feedback derived from the MUs firing rates were conducted. In both tasks, there was no evidence that participants were able to change MU firing rates in a way that would violate rigid control robustly. Our findings demonstrate limited flexibility in MU control in human tibialis anterior muscle within single-session training, even when real-time MU activity feedback was provided. The results suggest that MU flexibility is not inherently present in the human lower limb.

neuroscience↗

bioRxiv2023

Control limitations in the null-space of the wrist muscle system

The redundancy present within the musculoskeletal system may offer a non-invasive source of signals for movement augmen tation, where the muscle-to-force null-space could be controlled simultaneously to the natural limbs. Here, we investigated the viability of extracting movement augmentation control signals from the muscles of the wrist complex. Our study assessed i) if controlled variation of the muscle activation patterns in the wrist joints null-space is possible; and ii) whether force and null-space targets could be reached simultaneously. During the null-space target reaching condition, participants used EMG-to-force null-space muscle activation to move their cursor towards a displayed target while minimising the exerted force as visualised through the cursors size. Initial targets were positioned to require natural co-contraction in the null-space and if participants showed a consistent ability to reach for their current target, they would rotate 5{degrees} incrementally to generate muscle activation patterns further away from their natural co-contraction. In contrast, during the concurrent target reaching condition participants were required to match a target position and size, where their cursor position was instead controlled by their exerted flexion-extension and radial-ulnar deviation, while its size was changed by their natural co-contraction magnitude. The results collected from 10 participants suggest that while there was variation in each participants co-contraction behaviour, most did not possess the ability to control this variation for muscle-to-force null-space reaching. In contrast, participants did show a direction and target size dependent ability to vary isometric force and co-contraction activity concurrently. Our results show the limitations of using null-space activity in joints with a low level of redundancy.

neuroscience↗

bioRxiv2021

Unraveling the roles of Mast4 in amelogenesis via regulating DLX3 and stem cell maintenance of mouse incisors

Asymmetric division of stem cells allows for maintenance of the cell population and differentiation for harmonious progress. Developing mouse incisors allows for examination of how the stem cell niche employs specific insights into essential phases. Microtubule-associated serine/threonine kinase family member 4 (Mast4) knockout (KO) mice showed abnormal incisor development with weak hardness as the apical bud was reduced and preameloblasts were shifted to the apical side, resulting in Amelogenesis Imperfecta. In addition, Mast4 KO incisors showed abnormal enamel maturation, and stem cell maintenance was inhibited as amelogenesis accelerated. Distal-Less Homeobox 3 (DLX3), known to be a critical factor Tricho-Dento-Osseous (TDO) syndrome, is considered to be responsible for Amelogenesis Imperfecta in humans. MAST4 directly binds to DLX3 and induces phosphorylation at three residues within the nuclear localization sites (NLS) that promote the nuclear translocation of DLX3. MAST4-mediated phosphorylation of DLX3 ultimately controls the transcription of DLX3 target genes, which are carbonic anhydrase and ion transporter genes involved in the pH regulation process during ameloblast maturation. Taken together, our data reveal a novel role of MAST4 as a critical regulator of ameloblast maturation, which controls DLX3 transcriptional activity.

developmental biology↗