초록 ▼

Ⅳ. 연구개발결과
1. SCI 논문 3건:
(1) Sakuraba Y, Kim YS, Yoo SC, H†rtensteiner S, Paek NC (2013)7-Hydroxymethyl chlorophyll a reductase functions in metabolic channeling of chlorophyll breakdown intermediates during leaf senescence. Biochem. Biophys. Res. Commun. 430(1):32-37.
(2) Kim YS, Sakuraba Y

Ⅳ. 연구개발결과
1. SCI 논문 3건:
(1) Sakuraba Y, Kim YS, Yoo SC, H†rtensteiner S, Paek NC (2013)7-Hydroxymethyl chlorophyll a reductase functions in metabolic channeling of chlorophyll breakdown intermediates during leaf senescence. Biochem. Biophys. Res. Commun. 430(1):32-37.
(2) Kim YS, Sakuraba Y, Han SH, Yoo SC, Paek NC (2013) Mutation of the Arabidopsis NAC016 transcription factor delays leaf senescence. Plant Cell Physiol. 54(10):1660-1672.
(3) Sakuraba Y, Park SY, Kim YS, Wang SH, Yoo SC, H†rtensteiner S, Paek NC (2014) Arabidopsis STAY-GREEN2 Is a negative regulator of chlorophyll degradation during leaf senescence. Mol. Plant 7(8): 1288-1302.
2. 국내특허 출원 2건:
(1) NAC016 유전자를 이용한 비생물적 스트레스 내성이 증가된 기능성 녹색지속 변이식물체 제조 방법 및 그에 따른 식물체 (출원일자: 2013.08.13, 출원번호:10-2013-0095993)
(2) AtSGR2 유전자를 이용한 비생물적 스트레스 내성이 증가된 녹색 지속 변이 식물체의 제조 방법 및 그에 따른 식물체 (출원일자: 2014.03.05. 출원번호: 10-2014-0025914)

Abstract ▼

During natural or dark-induced senescence, chlorophyll degradation causes leaf yellowing. Recent evidence indicates that chlorophyll catabolic enzymes (CCEs) interact with the photosynthetic apparatus; for example, five CCEs (NYC1, NOL, PPH, PAO and RCCR) interact with LHCII. STAY-GREEN (SGR) and CC

During natural or dark-induced senescence, chlorophyll degradation causes leaf yellowing. Recent evidence indicates that chlorophyll catabolic enzymes (CCEs) interact with the photosynthetic apparatus; for example, five CCEs (NYC1, NOL, PPH, PAO and RCCR) interact with LHCII. STAY-GREEN (SGR) and CCEs interact with one another in senescing chloroplasts; this interaction may allow metabolic channeling of potentially phototoxic chlorophyll breakdown intermediates. 7-Hydroxymethyl chlorophyll a reductase (HCAR) also acts as a CCE, and HCAR interacted with LHCII in in vivo pull-down assays, and with SGR, NYC1, NOL and RCCR in yeast two-hybrid assays, indicating that HCAR is a component of the proposed SGR-CCE-LHCII complex, which acts in chlorophyll breakdown. In addition to SGR1, the Arabidopsis thaliana genome contains an additional homolog, SGR2 (At4g11910). Under senescence-inducing conditions, SGR2 expression is highly up-regulated, similarly to SGR1 expression.
Interestingly, SGR2 function counteracts SGR1 activity in leaf Chl degradation; SGR2-overexpressing plants stayed green and the sgr2-1 knockout mutant exhibited early leaf yellowing under age-, dark-, and stress-induced senescence conditions. Like SGR1, SGR2 interacted with LHCII but, in contrast to SGR1, SGR2 interactions with CCEs were very limited. Furthermore, SGR1 and SGR2 formed homo- or heterodimers, strongly suggesting a role for SGR2 in negatively regulating Chl degradation by possibly interfering with the proposed CCE-recruiting function of SGR1. The highly ordered process of senescence forms the final stage of leaf development; a large set of senescence-associated genes (SAGs) execute this orderly dismantling of the photosynthetic apparatus and remobilization of cellular components.A number of transcription factors (TFs) modulate SAG expression to promote or delay senescence.
NAC016, the previously uncharacterized senescence-associated NAM/ATAF1/2/CUC2 (senNAC) TF in Arabidopsis thaliana, promotes senescence. Leaves of nac016 mutants remained green under senescence-inducing conditions, and leaves of NAC016-overexpressing (NAC016-OX) plants senesced early. Under dark-induced senescence (DIS) conditions, nac016 mutants had low ion leakage, and retained the proper balance of photosystem proteins and normal grana thylakoid shape much longer than wild-type plants, suggesting that nac016 acts as a functional stay-green type senescence mutant. Under DIS conditions, SAGs (NYC1, PPH, SGR1/NYE1 and WRKY22), including senNACs (JUB1, NAP, ORE1, ORS1 and VNI2), were down-regulated in nac016 mutants and up-regulated in NAC016-OX plants.
In addition to its role in senescence, NAC016 also affects abiotic stress. Under salt and oxidative stress conditions, NAC016 expression rapidly increased in developing leaves, possibly to promote senescence. Indeed, under the stress conditions, nac016 mutants stayed green and NAC016-OX plants senesced rapidly.To identify direct targets of the NAC016 TF in the regulation of leaf senescence, we conducted yeast one-hybrid assays, which strongly suggested that NAC016 binds to the promoters of NAP and ORS1. Based on these results, NAC016 regulatory mechanisms promoting leaf senescence exhibit cross-talk with the salt and oxidative stress-responsive signaling pathways.