Tentative evidence indicates that a discrete tussock may not be genetically uniform, especially if its vitality is reduced. Using molecular markers, we studied the genetic composition of eight vigorous and eight weak tussocks of Carex sempervirens (cover !75% and 35%, respectively) to elucidate the relationship between tussock vigor and genetic variability. Four C. sempervirens tussocks harbored more than one genotype. However, all four variable tussocks were weak, and the additional genotypes occurred only at the edge of the tussock base. The formation of a genetically variable tussock of C. sempervirens is best explained by a seedling or small tussock being incorporated by a large, expanding tussock that eventually surrounds it. The vitalityrelated pattern was most likely caused by the greater intraspecific competition both inside and around the vigorous tussocks. We conclude that the formation of a tussock may involve more than one seedling and that tussocks, therefore, may not a priori be treated as genetic individuals.
Endogenous DNA double-strand breaks (DSBs) formation and repair in neural stem/progenitor cells (NSPCs) play fundamental roles in neurogenesis and neurodevelopmental disorders. NSPCs exhibit heterogeneity in terms of lineage fates and neurogenesis activity. Whether NSPCs also have heterogeneous regulations on DSB formation and repair to accommodate region-specific neurogenesis has not been explored. Here, we identified a regional regulator Filia, which is predominantly expressed in mouse hippocampal NSPCs after birth and regulates DNA DSB formation and repair. On one hand, Filia protects stalling replication forks and prevents the replication stress-associated DNA DSB formation. On the other hand, Filia facilitates the homologous recombination–mediated DNA DSB repair. Consequently, Filia−/− mice had impaired hippocampal NSPC proliferation and neurogenesis and were deficient in learning, memory, and mood regulations. Thus, our study provided the first proof of concept demonstrating the region-specific regulations of DSB formation and repair in subtypes of NSPCs.
Replication stress is a major source of endogenous DNA damage. Despite the identification of numerous proteins on replication forks to modulate fork or replication machinery activities, it remains unexplored whether noncoding RNAs can localize on stalled forks and play critical regulatory roles. Here, we identify an uncharacterized long noncoding RNA NONMMUT028956 (
Lnc956
for short) predominantly expressed in mouse embryonic stem cells.
Lnc956
is accumulated on replication forks to prevent fork collapse and preserve genomic stability and is essential for mouse embryogenesis. Mechanistically, it drives assembly of the
Lnc956
-TRIM28-HSP90B1 complex on stalled forks in an interdependent manner downstream of ataxia telangiectasia and Rad3-related (ATR) signaling.
Lnc956
-TRIM28-HSP90B1 complex physically associates with minichromosome maintenance proteins 2 (MCM2) to minichromosome maintenance proteins 7 (MCM7) hexamer via TRIM28 and directly regulates the CDC45-MCM-GINS (CMG) helicase retention on chromatin. The regulation of
Lnc956
-TRIM28-HSP90B1 on CMG retention is mediated by HSP90B1’s chaperoning function. These findings reveal a player that actively regulates replisome retention to prevent fork collapse.
Replication stress is a major source of endogenous DNA damage. Despite that numerous proteins have been identified on replication forks to modulate fork or replication machinery activities, it remains unexplored whether non-coding RNAs can localize on stalled forks and play critical regulatory roles. Here we identify an uncharacterized lncRNA NONMMUT028956 (Lnc956 for short) predominantly expressed in mouse embryonic stem cells. Lnc956 is recruited to stalled replication forks to prevent fork collapse and preserve genomic stability, and is essential for mouse embryogenesis. Mechanistically, it drives assembly of the Lnc956-TRIM28-HSP90B1 ribonucleoprotein (RNP) complex on stalled forks in an inter-dependent manner downstream of ATR signaling. This RNP complex physically associates with MCM2-7 hexamer via TRIM28 and directly regulates the CMG helicase retention on chromatin. The regulation of RNP on CMG retention is mediated by HSP90B1's chaperoning function. These findings reveal a novel pathway which actively regulates replisome retention to prevent fork collapse.
This study was to analyze the clinical application value of magnetic resonance imaging (MRI) image features based on intelligent algorithms in the diagnosis and treatment of breast cancer and to provide an effective reference assessment for breast cancer diagnosis. The MRI diagnosis model (ACO-MRI) based on the ant colony algorithm (ACO) was proposed, which was compared with the diagnosis methods based on support vector machine (SVM) and proximity (KNN) algorithm, and the proposed algorithm was applied to MRI images to diagnose breast cancer. The results showed that the accuracy, sensitivity, and specificity of the ACO-MRI model were greater than those of the KNN and SVM algorithm. Moreover, the specificity was statistically considerable compared with the two algorithms of KNN and SVM (
P
<
0.05
). By comparing 1/5 number of ants and the average gray path of the ACO-MRI model under 1/8 number of ants, it was found that the average gray path value of 1/8 number of ants was greatly higher than the average gray path value of 1/5 number of ants (
P
<
0.05
). The differences in the overall distribution of breast MRI imaging features among Luminal A, Luminal B, HER-2 overexpression, and TN were compared. There were considerable differences in the overall distribution of the three breast MRI imaging features of the boundaries, morphology, and enhancement methods among the four groups (
P
<
0.05
). In short, MRI image based on the intelligent algorithm ACO-MRI diagnosis model can effectively improve the diagnosis effect of breast cancer. Its image feature boundaries, morphology, and enhancement methods had good imaging features in the diagnosis of breast cancer.
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