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Viruses, as intracellular parasites, rely on the host organism to complete their life cycle. Although over 70% of plant viruses are transmitted by insect vectors, the role of vector energy metabolism on the infection process of insect-borne plant viruses is unclear. In this study, full-length cDNAs of three energy metabolism-related genes (LsATPase, LsMIT13 and LsNADP-ME) were obtained from the small brown planthopper (SBPH, Laodelphax striatellus), which transmits the Rice stripe virus (RSV). Expression levels of LsATPase, LsMIT13 and LsNADP-ME increased by 105%, 1120% and 259%, respectively, due to RSV infection. The repression of LsATPase, LsMIT13 or LsNADP-ME by RNAi had no effect on RSV nucleocapsid protein (NP) transcripts or protein levels. The repression of LsATPase caused a significant increase in LsMIT13 and LsNADP-ME transcript levels by 230% and 217%, respectively, and the repression of LsMIT13 caused a significant increase in LsNADP-ME mRNA levels. These results suggested that the silencing of LsATPase induced compensatory upregulation of LsMIT13 and LsNADP-ME, and silencing LsMIT13 induced compensatory upregulation of LsNADP-ME. Further study indicated that the co-silencing of LsATPase, LsMIT13 and LsNADP-ME in viruliferous SBPHs increased ATP production and RSV loads by 182% and 117%, respectively, as compared with nonviruliferous SBPHs. These findings indicate that SBPH energy metabolism is involved in RSV infection and provide insight into the association between plant viruses and energy metabolism in the insect vector. [ABSTRACT FROM AUTHOR]

PIWI‐interacting RNAs (piRNAs) are abundantly expressed in heart. However, their functions and molecular mechanisms during myocardial infarction remain unknown. Here, a heart‐apoptosis‐associated piRNA (HAAPIR), which regulates cardiomyocyte apoptosis by targeting N‐acetyltransferase 10 (NAT10)‐mediated N4‐acetylcytidine (ac4C) acetylation of transcription factor EC (Tfec) mRNA transcript, is identified. HAAPIR deletion attenuates ischemia/reperfusion induced myocardial infarction and ameliorate cardiac function compared to WT mice. Mechanistically, HAAPIR directly interacts with NAT10 and enhances ac4C acetylation of Tfec mRNA transcript, which increases Tfec expression. TFEC can further upregulate the transcription of BCL2‐interacting killer (Bik), a pro‐apoptotic factor, which results in the accumulation of Bik and progression of cardiomyocyte apoptosis. The findings reveal that piRNA‐mediated ac4C acetylation mechanism is involved in the regulation of cardiomyocyte apoptosis. HAAPIR‐NAT10‐TFEC‐BIK signaling axis can be potential target for the reduction of myocardial injury caused by cardiomyocyte apoptosis in ischemia heart diseases. [ABSTRACT FROM AUTHOR]

To develop an efficient method for rescuing I TENT5D i -associated sterility, we tested the "FACS + ROSI" strategy in the I Tent5d i -mutated mouse model. Similarly, ICSI for I Tent5d i -mutated male mice was also inefficient, limiting its potential application in overcoming I TENT5D i -associated male infertility (Supplementary Fig. Furthermore, the success of the "FACS + ROSI" approach in I Tent5d i -mutated male mice indicates an effective treatment for human male infertility caused by I TENT5D i mutations. [Extracted from the article]

Glioma is a common type of tumor originating in the brain. Glioma develops in the gluey supporting cells (glial cells) that surround and support nerve cells. Exosomes are extracellular vesicles that contain microRNAs, messenger RNA, and proteins. Exosomes are the most prominent mediators of intercellular communication, regulating, instructing, and re-educating their surrounding milieu targeting different organs. As exosomes' diameter is in the nano range, the ability to cross the blood–brain barrier, a crucial obstacle in developing therapeutics against brain diseases, including glioma, makes the exosomes a potential candidate for delivering therapeutic agents for targeting malignant glioma. This review communicates the current knowledge of exosomes' significant roles that make them crucial future therapeutic agents and diagnostic tools for glioma. [ABSTRACT FROM AUTHOR]