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<span style="font-family: "Book Antiqua", serif; font-size: 24pt; color: black;"> Yunde Zhao</span><span style="font-family: "Gill Sans", sans-serif; font-size: 18pt; color: rgb(0, 74, 172);"> </span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 11pt; color: rgb(0, 74, 172);">Professor, Cell and Developmental Biology</span></p>
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University of California San Diego</div>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 18pt; color: rgb(0, 74, 172); background-color: white;">Molecular mechanisms of auxin-mediated flower initiation</span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 16pt; color: black;"> </span><span style="font-family: "Gill Sans", sans-serif; font-size: 12pt; color: black;"><b> Date:</b> Friday, December 6</span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 12pt; color: black;"> <b>Time:</b> 12pm - 1:00 pm</span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 12pt; color: black;"> <b> Location:
</b>Genomics Auditorium 1102</span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 12pt; color: black;"><b>Abstract:</b></span></p>
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<span style="font-family: "Gill Sans", sans-serif; font-size: 12pt; color: black;">Auxin is required for normal development of flowers. Several Arabidopsis mutants fail to produce flowers after transition from vegetative growth to reproductive phase, resulting
in the formation of pin-like inflorescences. Among the mutants, pin-formed 1 (pin1) is defective in polar auxin transport. A similar mutant called pinoid (pid) also develops pin-like inflorescences and PID encodes a Ser/Thr protein kinase. A prominent dogma
is that PID phosphorylates PIN1to regulate PIN polarity and activities. We cloned a family of genes (NPYs) that phenocopies of pid and pin1 when compromised. The npy1 was isolated as an enhancer of yuc1 yuc4 double mutants, which are defective in auxin biosynthesis.
We showed that npy1 npy2 npy5 triple mutants and npy1 yuc1 yuc4 triple mutants developed strong pin-like inflorescences. How PIN1, PID, NPY, and YUCs are connected at the molecular level is not understood. In this presentation, I will show that new genetic
materials we generated using CRISPR/cas9 has revealed unexpected relationships among the aforementioned genes. For example, we inserted green fluorescent protein (GFP) into the hydrophilic loop of PIN1 through CRISPR-mediated homology-directed repair (HDR).
The GFP signal and pattern in the PIN1-GFPHDR line are similar to those in the previously reported PIN1-GFP transgenic lines. However, the PIN1-GFPHDR line rescued various pid null mutant alleles in a semi-dominant fashion. Moreover, we show that pid phenotypes
are suppressed by heterozygous pin1 mutants, a result that is not consistent with the current dogma that PID phosphorylates and activates PIN1. I will provide our updated upstanding of the relationships among the aformentioned PIN1, PID, and NPY gene</span></p>
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