Identification, classification, and expression profiles of heat shock transcription factors in tea plant (Camellia sinensis) under temperature stress

Abstract Background Both APETALA2/Ethylene Responsive Factor (AP2/ERF) superfamily and R2R3-MYB family were from one of the largest diverse families of transcription factors (TFs) in plants, and played important roles in plant development and responses to various stresses. However, no systematic analysis of these TFs had been conducted in the green algae A. protothecoides heretofore. Temperature was a critical factor affecting growth and lipid metabolism of A. protothecoides. It also remained largely unknown whether these TFs would respond to temperature stress and be involved in controlling lipid metabolism process. Results Hereby, a total of six AP2 TFs, six ERF TFs and six R2R3-MYB TFs were identified and their expression profiles were also analyzed under low-temperature (LT) and high-temperature (HT) stresses. Meanwhile, differential adjustments of lipid pathways were triggered, with enhanced triacylglycerol accumulation. A co-expression network was built between these 18 TFs and 32 lipid-metabolism-related genes, suggesting intrinsic associations between TFs and the regulatory mechanism of lipid metabolism. Conclusions This study represented an important first step towards identifying functions and roles of AP2 superfamily and R2R3-MYB family in lipid adjustments and response to temperature stress. These findings would facilitate the biotechnological development in microalgae-based biofuel production and the better understanding of photosynthetic organisms’ adaptive mechanism to temperature stress.

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Two MYB transcription factors (CsMYB2 and CsMYB26) are involved in flavonoid biosynthesis in tea plant [Camellia sinensis (L.) O. Kuntze]

BMC Plant Biology ◽

10.1186/s12870-018-1502-3 ◽

2018 ◽

Vol 18 (1) ◽

Cited By ~ 17

Author(s):

Wen-Li Wang ◽

Yong-Xin Wang ◽

Hui Li ◽

Zhi-Wei Liu ◽

Xin Cui ◽

...

Keyword(s):

Transcription Factors ◽

Camellia Sinensis ◽

Tea Plant ◽

Flavonoid Biosynthesis ◽

Myb Transcription Factors

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Differential Expression of Heat Shock Transcription Factors and Heat Shock Proteins after Acute and Chronic Heat Stress in Laying Chickens (Gallus gallus)

PLoS ONE ◽

10.1371/journal.pone.0102204 ◽

2014 ◽

Vol 9 (7) ◽

pp. e102204 ◽

Cited By ~ 47

Author(s):

Jingjing Xie ◽

Li Tang ◽

Lin Lu ◽

Liyang Zhang ◽

Lin Xi ◽

...

Keyword(s):

Transcription Factors ◽

Heat Stress ◽

Heat Shock ◽

Heat Shock Proteins ◽

Differential Expression ◽

Gallus Gallus ◽

Heat Shock Transcription Factors ◽

Shock Proteins

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Rescue of a developmental arrest caused by a C. elegans heat-shock transcription-factor mutation by loss of ribosomal S6-kinase activity

10.1101/310086 ◽

2018 ◽

Author(s):

Peter Chisnell ◽

T. Richard Parenteau ◽

Elizabeth Tank ◽

Kaveh Ashrafi ◽

Cynthia Kenyon

Keyword(s):

Transcription Factor ◽

Transcription Factors ◽

Heat Shock ◽

Heat Shock Transcription Factor ◽

Adult Longevity ◽

Loss Of Function ◽

S6 Kinase ◽

Heat Shock Transcription Factors ◽

C Elegans ◽

Developmental Arrest

AbstractThe widely conserved heat-shock response, regulated by heat shock transcription factors, is not only essential for cellular stress resistance and adult longevity, but also for proper development. However, the genetic mechanisms by which heat-shock transcription factors regulate development are not well understood. In C. elegans, we conducted an unbiased genetic screen to identify mutations that could ameliorate the developmental arrest phenotype of a heat-shock factor mutant. Here we show that loss of the conserved translational activator rsks-1/S6-Kinase, a downstream effector of TOR kinase, can rescue the developmental-arrest phenotype of hsf-1 partial loss-of-function mutants. Unexpectedly, we show that the rescue is not likely caused by reduced translation, nor to activation of any of a variety of stress-protective genes and pathways. Our findings identify an as-yet unexplained regulatory relationship between the heat-shock transcription factor and the TOR pathway during C. elegans’ development.

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