【文献解读】NATURE COMMUNICATIONS：ChIP

背景：

SARD1：SAR DEFICIENT1

CBP60g：CAM-BINDING PROTEIN60-LIKE G

SARD1 and CBP60g arepositive regulatorsof systemic immunity andsignalling components for effector-triggered immunity and PAMP-triggered immunity.

Arabidopsis SNC2 encodes an receptor-likeprotein that is required for resistance against pathogenic bacteria Pseudomonassyringae pv tomato (P.s.t.) DC3000 and non-pathogenic

bacteria P. syringae pv tomato DC3000 hrcC.A gain-of-function mutation in snc2-1D leads to constitutive activation of bothSA-dependent and SA-independent defence pathways.

Isochorismate Synthase 1 (ICS1), which is akey enzyme in pathogen-induced SA synthesis.

EDS5（ENHANCED DISEASE

SUSCEPTIBILITY 5）encodes a transporter involved in exporting SA from chloroplast tocytoplasm.

NPR1（NON-EXPRESSOR OF

PATHOGENESIS RELATED GENES1, a gene required for the perception of SA by plants）and itsparalogs, NPR3 and NPR4,bind to SA and may function as SA receptors.

FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1)encodes a putative monooxygenase13–15, AGD2-LIKE DEFENSE RESPONSE PROTEIN1(ALD1) encodes an aminotransferase16, and avrPphB SUSCEPTIBLE3 (PBS3) encodes amember of the firefly luciferase superfamily.These genes are essential for SAR(systemicacquired resistance).

结果：

主要通过ChIP-seq筛选到SARD1 and CBP60g的靶基因，通过ChIP-qPCR以及定量进行验证，发现其可以调控与SAR(systemic acquired resistance)，ETI 及PTI正向调控相关基因；还发现SARD1

and CBP60g可结合一些免疫负调控基因，推测是与SA反馈抑制相关，避免自身免疫。另外还通过分析发现二者的结合元件GAAATTT，利用luciferase reporter gene进行验证。

日积月累：

Calmodulin n. [生化] 钙调蛋白；携钙素

Autoimmunity n. [免疫] 自身免疫；[免疫] 自身免疫性

1.Recognition of pathogens by host plants leads to rapid

transcriptional reprogramming and

activation of defence responses.

2.Plants use a multilayereddefence system to combat microbial pathogens.

3.These data suggest thatSARD1 and CBP60g haveoverlapping functionsin regulatingthe expression of WRKY70.

题外话：有没有了解ChIP-qPCR的童鞋，文献看完但还是不清楚这个实验怎么做的，求指点，谢谢。