rotor, 4 x 100ml economy
- Known as:
- rotor, 4 x 100ml economy
- Catalog number:
- C0326-12
- Category:
- -
- Supplier:
- Labne
- Gene target:
- rotor 4 100ml economy
Related genes to: rotor, 4 x 100ml economy
- Gene:
- PRR5 NIH gene
- Name:
- proline rich 5
- Previous symbol:
- -
- Synonyms:
- PP610, FLJ20185k, Protor-1
- Chromosome:
- 22q13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-16
- Date modifiied:
- 2016-10-05
Related products to: rotor, 4 x 100ml economy
Related articles to: rotor, 4 x 100ml economy
- Root hairs, derived from trichoblasts, are critical for plant growth and environmental adaptation. Although environmental cues are known to influence root hair development, how endogenous timing systems such as the circadian clock integrate into the core transcriptional network governing root hair formation remains unclear. Here, we show that the circadian clock-associated protein PSEUDO-RESPONSE REGULATOR5 (PRR5) physically interacts with ROOT HAIR DEFECTIVE6 (RHD6) and RHD6 LIKE1 (RSL1), two basic helix-loop-helix transcription factors essential for root hair initiation. Genetic analyses suggest that PRR proteins contribute to root hair development under long-day conditions in Arabidopsis thaliana. Simultaneous disruption of PRR5, PRR7, and PRR9 results in defective root hairs, whereas PRR5 overexpression markedly increases root hair density and length. Transcriptomic and RT-qPCR analyses reveal that PRRs enhance the expression of RHD6, RSL1, and multiple downstream root hair-responsive genes, while modulating their temporal expression patterns. Furthermore, PRR5-mediated root hair promotion requires RHD6/RSL1, and PRR proteins enhance RHD6-dependent activation of the RSL4 promoter. PRRs also contribute to root hair development under phosphate-deficient and salt-stress conditions. Together, these findings establish a molecular framework in which PRR proteins regulate the RHD6/RSL network to coordinate root hair development and environmental responses. - Source: PubMed
Publication date: 2026/08/21
Bai NingZhao YanWang TianmeiLi MinchenHan XiaoYang MilianZhou LijuanYe YajinZhang ZhiqiangHu YanruHe Kunrong - High ambient temperature accelerates soybean (Glycine max) flowering to escape stress and accomplish reproduction, but the underlying molecular mechanism remains unclear. Here, we report that phytochrome B1 (phyB1) and phyB2 and the core circadian-clock components PRR5a and PRR5b regulate high-temperature-mediated early flowering. PRR5a and PRR5b repress FLOWERING LOCUS T (FT)2a and FT5a expression by directly binding to their promoters. Under high temperature, enhanced phyB and PRR5 interaction promotes PRR5 degradation, facilitating FT induction and precocious flowering. prr5a prr5b and phyB1 phyB2 double mutants showed temperature-insensitive flowering at 25°C and 30°C. PRR5a and PRR5b are epistatic to phyB1 and phyB2, and this circuit bypasses the E1 photoperiod module to promote flowering. Taken together, this study uncovers a phyB-PRR5-FT module controlling high-temperature-mediated early flowering, broadening our understanding of plants' adaptation strategies for maximizing reproductive success under environmental stress. - Source: PubMed
Publication date: 2026/03/20
Hou ZhihongLi HaiyangTang YangZhang KeLi LanxinGou ChuanjieHe MilanSun ZhihuiZheng ChengwenLiu BaohuiLi HongLin XiaoyaKong FanjiangLiu Huan - The circadian clock is an endogenous timekeeping mechanism that coordinates diverse biological processes across diverse organisms. Emerging evidence recently underscores its critical role in modulating plant immune responses. Salicylic acid (SA) is a central phytohormone in plant immunity; however, the molecular mechanisms by which clock components influence SA signaling under biotic stress are poorly understood. Here, we report the pivotal role of the core clock components, PSEUDO-RESPONSE REGULATOR 5 (PRR5) and PRR7, in governing Arabidopsis immunity by direct suppression of SA signaling. We found that the transcriptional outputs of SA signaling showed rhythmic expression and were remarkably affected by PRR5 and PRR7. Genetic analyses revealed that PRR5 and PRR7 function genetically upstream of the SA receptor NONEXPRESSER OF PATHOGENESIS-RELATED GENES 1 (NPR1) to inhibit SA-mediated defenses. Biochemical assays confirmed physical interactions among PRR5/7, NPR1, and TGA3, highlighting a direct mechanism whereby PRR5/7 antagonize the transcriptional activity of the NPR1-TGA3 complex. The prr5 prr7 double mutant not only showed enhanced SA signaling but also boosted pathogen-associated molecular pattern-triggered immunity, highlighting their broad inhibitory function in plant immunity. These findings provide critical insights into the temporal dynamics of plant immunity and reveal key molecular targets for breeding crop varieties with an optimized balance between growth and immunity. - Source: PubMed
Publication date: 2026/02/25
Li ShaoqinWang HailinYe ZumeiFu ZhijuRu YanyuYang YongpingWu KongfenYu DiqiuJiang Yanjuan - YTH domain family protein 2 (YTHDF2), a decay-promoting N-methyladenosine (mA) binding protein, determines the fate of modified mRNA, acting as a key effector downstream of mA methyltransferases and demethylases. However, how the interplay between YTHDF2 and mA methyltransferases/demethylases regulates arsenic carcinogenesis remains unknown. In this study, using both in vitro (human keratinocytes treated with 1 μM arsenite for 24 weeks) and in vivo (mice exposed to 10 mg/kg/day for 12 weeks) models, we report an mA-dependent mechanism through which YTHDF2 promotes arsenic carcinogenesis by activating pro-cancer signaling and suppressing anti-cancer signaling. Integrative multi-omics analyses combining time-course mRNA-seq, MeRIP-seq, and computational prediction of YTHDF2 targets identified PRR5 and SMAD7 as key YTHDF2-associated transcripts implicated in arsenic carcinogenesis. Global mA levels increased by 2.38-fold (24 weeks) in keratinocytes and by 3.22-fold (12 weeks) in mouse skin. Mechanistically, the mA methyltransferase METTL3 enhanced YTHDF2-mediated destabilization of SMAD7 mRNA by increasing mA on SMAD7 transcripts. In contrast, the mA demethylase fat mass and obesity-associated protein (FTO) reduced mA on PRR5, thereby weakening YTHDF2 engagement, which allows PRR5 to escape YTHDF2-mediated decay and accumulate. Site-specific SELECT-qPCR further validated dynamic mA remodeling at site 1347 of PRR5 and site 2441 of SMAD7. Functionally, YTHDF2 promoted malignant phenotypes in keratinocytes and exacerbated arsenic-induced skin lesions in mice, accompanied by activation of the PRR5-mTORC2-AKT axis and enhancement SMAD2/3 signaling. This study advances our understanding of how opposing mA regulatory axes shape YTHDF2 engagement and mRNA decay outputs, thereby promoting arsenic carcinogenesis by regulating oncogenic and tumor-suppressive signaling. - Source: PubMed
Publication date: 2026/02/09
Zhang QianMan JinCai JingsilinZhao TianheZhang Zunzhen - Triple-negative breast cancers (TNBCs) lack targeted therapeutics that can inhibit their growth and progression. The long intergenic noncoding RNA LINC01133 promotes TNBC pathogenesis by increasing the abundance of proline-rich protein 5 (PRR5), an mTORC2 component that activates the kinase AKT in a PI3K-independent, mTORC2-dependent manner. Here, however, we found that TNBC cell proliferation was incompletely sensitive to AKT inhibitors alone because PRR5 also stimulated the mitogen-activated protein kinase (MAPK) cascade in an mTORC2-dependent manner. PRR5 associated with and prevented the ubiquitin-dependent proteasomal degradation of IQGAP1, an adaptor protein that promotes activation of the MAP kinase ERK. ERK signaling was essential for LINC01133-mediated TNBC proliferation in two- and three-dimensional cultures, and ERK inhibitors synergized with AKT blockade to suppress LINC01133-induced TNBC cell growth. Furthermore, PRR5 abundance was particularly enriched and correlated with that of phosphorylated ERK in samples from patients with TNBC. Our results highlight cross-talk between mTORC2 and ERK signaling downstream of LINC01133 and PRR5 that may be therapeutically targeted to treat TNBC. - Source: PubMed
Publication date: 2026/02/10
Tu ZhenboMoses LeahHu YiSapkota SworajQuintana Liza MGuerrero LeismiBell George WKarnoub Antoine E