76 research outputs found
μ¬ννμν¨μλ₯Ό μ΄μ©ν λμκ΅ν΅μ μ± μ ννμ± λΆμ
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Όλ¬Έ (λ°μ¬)-- μμΈλνκ΅ νκ²½λνμ νκ²½κ³ννκ³Ό, 2017. 8. κΉμ±μ.κ΅λ΄μμλ λ€μν λΆμΌμμ ννμ± λ¬Έμ μ λν μ°κ΅¬κ° μ§νλκ³ μμΌλ©°, κ΅ν΅ λΆμΌμμλ λ
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Abstract 143Docto
Photoprotective effect of various sunscreens against ultraviolet B-induced chronic skin damage
μνκ³Ό/μμ¬[νκΈ]
λ§μ±μ μΈ μμΈμ λ
ΈμΆμ νΌλΆμ κ΅΅κ³ κΉμ μ£Όλ¦κ³Ό μ¬ν κ±°μΉ μ, λΆκ· μΌν μμμΉ¨μ°© λ±μ κ΄λ
Ένμ νΌλΆμμ μ λ°ν μ μλ€. Albino hairless Skh:HR-1 mouseλ μμΈμ μ μν νΌλΆμμμ μ°κ΅¬νλ μ¬λ£λ‘μ¨ λ리 μ¬μ©λκ³ μμΌλ©°, μμΈμ μ μν νΌλΆμμμ μ λ
μΈ‘μ μΉλ‘μ¨ μ‘μμ μ£Όλ¦ λ³ν λ° ννΌμ μ§νΌμΈ΅μ λνλλ μ‘°μ§νμ λ³νκ° μ΄μ©λκ³ μλ€. μμΈμ μ μν νΌλΆμμμ κ°μμν€λ €λ λ
Έλ ₯μΌλ‘ μμΈμ μ°¨λ¨μ μ λν¬κ° μκ°λμ΄ νμ¬ μΌκ΄νμκ³Ό κ°μ μμΈμ μ μν κΈμ± μμμ λ°©μ§νκΈ° μν΄ μ¬μ©λκ³ μλ€.
λ³Έ μ°κ΅¬μ μλ albino hairless Skh:HR-1 mouseλ₯Ό μ΄μ©νμ¬ μμΈμ Bλ₯Ό μ₯κΈ°κ° μ‘°μ¬νμ¬ λνλλ μ‘μμ μ£Όλ¦ λ³νμ μ’
μ λ°μ λ° μ‘°μ§νμ λ³νλ₯Ό κ΄μ°°νκ³ , κ·μΉμ μΌλ‘ μμΈμ μ°¨λ¨μ λ₯Ό λν¬ν μ€νκ΅°κ³Ό μμΈμ μ°¨λ¨μ λ₯Ό λν¬νμ§ μκ³ μμΈμ Bλ₯Ό μ‘°μ¬ν λμ‘°κ΅°
μ λΉκ΅νμ¬ λ€μκ³Ό κ°μ κ²°κ³Όλ₯Ό μ»μλ€.
1. μμΈμ 8μ λ
ΈμΆλ νΌλΆλ κΉκ³ κ΅΅μ ν‘μ£Όλ¦μ΄ λνλκ³ νλ©΄μ κ±°μΉ κ³ λκΊΌμμ§λ κ΄λ
Ένκ° κ΄μ°°λμλ€.
2. κ΄λ
Ένλ νΌλΆμ μ‘°μ§νμ μ견μ hematoxylin-eosin μΌμμ ννΌ λκ»κ° μ¦κ°νκ³ , μ§νΌλ΄ μ¬μ μμΈν¬μ μΌμ¦μΈν¬κ° μ¦κ°νμμΌλ©° λμ’
μ λ³νκ° κ΄μ°°λμλ€.
3. μμΈμ Bλ₯Ό μ‘°μ¬ν λ§μ°μ€ λ°°λΆμμ μ€νμ’
λ£μ μ΄ 9λ§λ¦¬ μ€ 7λ§λ¦¬(78%)μμ μ’
μλ―Έ κ΄μ°°λμμΌλ©°, μ‘°μ§νμ μΌλ‘ μ λμ’
μ견과 μ΄κ°νμΈν¬ λ° μΈν¬λ°°μ΄ κ·Ήμ±μ μμ€μ΄ κ΄μ°°λμλ€.
4. 0ctylmethoxycinnamateμ TiO^^2 .ZnO.Talcλ₯Ό ν¨μ ν μμΈμ μ°¨λ¨μ λ₯Ό λν¬ν νμνμ Bλ₯Ό μ‘°μ¬ν μ€νκ΅°μ κΈ°μ μ²μΉκ΅°μ΄λ μμΈμ μ°¨λ¨μ λ₯Ό λν¬νμ§ μκ³ μμΈμ Bλ₯Ό μ‘°μ¬ν λμ‘°κ΅°μ λΉνμ¬ μ‘μμ μ£Όλ¦ λ³νμ μ μκ° κ°μνμμΌλ©° μ‘°μ§νμ μΌλ‘ ννΌ λκ» μ¦κ°κ° λ―Έμ½νκ³ μ§νΌλ΄ μΈν¬μ μ¦κ° λ° λμ’
μ λ³ν μ λκ° κ°μνμλ€.
5. Octyl dimethyl para-aminobenzoic acid(PA8A)λ₯Ό ν¨μ ν μμΈμ μ°¨λ¨μ λ₯Ό λν¬νμ€νκ΅°μ κΈ°μ μ²μΉκ΅°μ΄λ μμΈμ μ°¨λ¨μ λ₯Ό λν¬νμ§ μκ³ μμΈμ Bλ₯Ό μ‘°μ¬ν λμ‘°κ΅°μ λΉνμ¬ μ‘μμ μ£Όλ¦ λ³νμ μ μμ μ§νΌλ΄ μΌμ¦μΈν¬ μΉ¨μ€μ΄ μ¦κ°νμλ€.
6. μ€νμ’
λ£μ Octyl metluxycinnamateλ₯Ό ν¨μ ν μμΈμ μ°¨λ¨μ μ²μΉκ΅°μμλ μ΄ 7λ§λ¦¬ μ€ 1λ§λ¦¬(14%)μ μ μ’
μμ΄ κ΄μ°°λμκ³ TiO^^2 , ZnO, Talcλ₯Ό ν¨μ ν μμΈμ μ°¨λ¨μ μ²μΉκ΅°μμλ μ’
μμ΄ κ΄μ°°λμ§ μμμΌλ©°, octl dimethyIPABAλ₯Ό ν¨μ ν μμΈμ μ°¨λ¨μ μ²μΉκ΅°μ μ΄ 7λ§λ¦¬ μ€ 5λ§λ¦¬(71%)μμ κ΄μ°°λμλ€.
μ΄μμ κ²°κ³Όλ‘ μμΈμ Bμ μ₯κΈ°κ° λ
ΈμΆλ νΌλΆλ κ΄λ
Ένμ μ’
μμ΄ λ°μν μ μμΌλ©°, κ·μΉμ μΈ μμΈμ μ°¨λ¨μ λν¬λ μμΈμ Bμ μν νΌλΆμμ μ λλ₯Ό κ°μμμΌ μ€ μ μμΌλ. μ μ ν μμΈμ μ°¨λ¨μ μ μ νμ΄ μ€μν κ²μΌλ‘ μκ°λλ€.
Photoprotective effect of various sunscreens against ultraviolet B-induced chronic
skin damage
Hyun Joo Choi
Department of Medical Science, The Graduate School Yonsei University
(Directed by Professor Yoon-Kee Park)
Chronic exposure to ultaviolet radiation(UVR) induces photoaging characterized by
dry, deeply wrinkled, inelastic, leathery, and irregularly pigmented skin. UVR also
induces solar keratosis and carcinoma, and is a contributing factor in melanoma.
The albino hairless Skh: HR-1 mouse has been used as a model to study the
photoaging effects of UVR in the skin. There are dramatic changes in appearance of
the skin surface such as wrinkling and sagging, in addition to the appearance of
skin tumors when they are exposed chronically to UVR. There are also a number of
histological alterations in the epidermis and dermis. These gross and microscopical
changes in the mouse skin -have been used as the markers of photodamage. Sunscreens
are used to prevent solar damage to skin and, if used on daily basis, should
significantly reduce the incidence of the chronic photodamaging events. In this
study we used the albino hairless Skh:HR-1 mousse exposed chronically to
ultraviilet B(UVB) to study the gross and microscopic changes in the skin, and the
photoprotective effect of various sunscreens.
The results are summarized as follows :
1. The skin of UVB-irradiated mouse shows characteristic signs of photoaging,
such as deep wrinkles across the back, and thickened and leathery skin.
2. Histologically, the photoaged skin shows increased epidermal thickness,
numerous fibroutlasts and inflammatory cell irfi1tration in user dermis, and many
enlarged keratinizing cysts in lower dermis.
3. At 20th week, seven of total 9 mice(78%) in UVB-irradiated mitre developed at
least one tumor. Histologically, the tumor is a papilloma, but there an many
dyskeratotic cells and loss of polarity in epidermis.
4. Octyl methoxycinnamate or TiO^^2 Β·ZnOΒ·Talc-treated mice show significanty
decreased wrinkling score, minimal epidermal hypcrplasia, slightly increased dermal
cellularity, and lack of proliferation of cysts.
5. Octyl dimethyl PABA-treated mouse slews significantly increased wrinkling
score and marked inflammatory infiltration in dermis.
6. At 20th week, only one mouse developed a tumor in octyl
methoxycinnamate-treated group and no evidence of tumor was seen in
TiO^^2 Β·ZnOΒ·Talc-treated group. In octyl dimethyl PABA-treated group, five of 7
mice(71%) developed at least one tumor.
From these results, the skin which is chronically exposed to UVB subject to
toaging and photocarcinogenesis and regular use of adequate sunscreen would prevent
these photodamaging effects of UVB,
[μλ¬Έ]
Chronic exposure to ultaviolet radiation(UVR) induces photoaging characterized by dry, deeply wrinkled, inelastic, leathery, and irregularly pigmented skin. UVR also induces solar keratosis and carcinoma, and is a contributing factor in melanoma.
The albino hairless Skh: HR-1 mouse has been used as a model to study the photoaging effects of UVR in the skin. There are dramatic changes in appearance of the skin surface such as wrinkling and sagging, in addition to the appearance of skin tumors when they are exposed chronically to UVR. There are also a number of histological alterations in the epidermis and dermis. These gross and microscopical changes in the mouse skin -have been used as the markers of photodamage. Sunscreens are used to prevent solar damage to skin and, if used on daily basis, should
significantly reduce the incidence of the chronic photodamaging events. In this study we used the albino hairless Skh:HR-1 mousse exposed chronically to ultraviilet B(UVB) to study the gross and microscopic changes in the skin, and the photoprotective effect of various sunscreens.
The results are summarized as follows :
1. The skin of UVB-irradiated mouse shows characteristic signs of photoaging, such as deep wrinkles across the back, and thickened and leathery skin.
2. Histologically, the photoaged skin shows increased epidermal thickness, numerous fibroutlasts and inflammatory cell irfi1tration in user dermis, and many enlarged keratinizing cysts in lower dermis.
3. At 20th week, seven of total 9 mice(78%) in UVB-irradiated mitre developed at least one tumor. Histologically, the tumor is a papilloma, but there an many dyskeratotic cells and loss of polarity in epidermis.
4. Octyl methoxycinnamate or TiO^^2 Β·ZnOΒ·Talc-treated mice show significanty decreased wrinkling score, minimal epidermal hypcrplasia, slightly increased dermal cellularity, and lack of proliferation of cysts.
5. Octyl dimethyl PABA-treated mouse slews significantly increased wrinkling score and marked inflammatory infiltration in dermis.
6. At 20th week, only one mouse developed a tumor in octyl
methoxycinnamate-treated group and no evidence of tumor was seen in TiO^^2 Β·ZnOΒ·Talc-treated group. In octyl dimethyl PABA-treated group, five of 7 mice(71%) developed at least one tumor.
From these results, the skin which is chronically exposed to UVB subject to toaging and photocarcinogenesis and regular use of adequate sunscreen would prevent these photodamaging effects of UVB,restrictio
μ‘°νμΈ‘λμ μΈκ² ν΅
Thesis (master`s)--μμΈλνκ΅ λνμ :μ리과νλΆ,2003.Maste
Expression of cell adhesion molecules and binding of T lymphocyte on human dermal microvascular endothelial cells b
μνκ³Ό/λ°μ¬[νκΈ]
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μ Treponema pallidum(T.pallidum)μ μν΄ λ€μν μμμμμ 보μ΄λ©°, λ³λ¦¬μ‘°μ§νμ μΌλ‘ νκ΄ λ΄νΌμΈν¬μ λ³νμ νκ΄μ£ΌμμΌ λ±μ μ견μ 보μ΄λ λ§μ± μ±μΈμ± μ§νμ΄λ€. νκ΄ λ΄νΌμΈν¬λ λ°±νꡬ μ΄λ, λ³΅κ· λ° μΌμ¦λ°μμμ μ€μν μν μ νλ€. νκ΄ λ΄νΌμΈν¬μ λν T λ¦Όνꡬμ μ μ°©μ μλ¬Όνμ λ°μ μ‘°μ λ¬Όμ§μ μν΄ μ‘°μ λλ©° intercellular cell adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1), E-selectin λ±μ μΈν¬μ μ°©λΆμμ μν΄ μ€κ°λλ€. 맀λ
λ³λ³μ μ΄μ μλ 맀λ
κ· μ체 λΏ μλλΌ λ§€λ
κ· μ νμμ λνμμ£Όμ λ©΄μλ°μμ μν΄μλ μ λ°λλ€. 맀λ
κ· 47 kDa νμμ 맀λ
κ· κ°μΌμ μ€μν μλ¬Όνμ μν μ ν κ²μΌλ‘ μμ¬λμ΄ μλ€. λ³Έ μ°κ΅¬μμλ 맀λ
κ· 47 kDa νμμ΄ λ§€λ
κ· κ°μΌμ λ°λ³κΈ°μ μ λ―ΈμΉλ μν μ μμλ³΄κ³ μ λ©΄μνκ΄ μ λ μΈν¬λΆμκ³Ό ν¨μ λ©΄μνμ§λ²μΌλ‘ 맀λ
κ· λ° λ§€λ
κ· 47kDa νμμ 첨κ°νκ³ λ°°μν μΈμ²΄ μ§νΌ λ―ΈμΈνκ΄ λ΄νΌμΈν¬(human dermal micro-vascular endothelial cells: HDMEC) νλ©΄ μΈν¬μ μ°©λΆμ λ°ν λ³νλ₯Ό κ΄μ°°νκ³ HDMECμ λν T λ¦Όνꡬ μ μ°©μ€νμ μννμ¬ λ€μκ³Ό κ°μ κ²°κ³Όλ₯Ό μ»μλ€.
1. T. pallidumμ 첨κ°νκ³ λ°°μν HDMEC νλ©΄μμ ICAM-1 λΆμ λ°νμ΄ μκ·Ή μ μ λΉν΄ μ μνκ² μ¦κ°νμκ³ , VCAM-1κ³Ό E-selectin λΆμ λ°νμ΄ κ΄μ°°λμμΌλ©°, μ΄λ¬ν μ μ°©λΆμμ λ°νμ 첨κ°ν T. pallidumμ μμ λΉλ‘νμ¬ μ¦κ°νμλ€.
2. λΉλ³μμ± κ· μ£ΌμΈ T. phagedenis, T. refringens, T.denticola νΉμ λΉνμ±νμν¨ T. pallidumμ 첨κ°νκ³ λ°°μν HDMEC νλ©΄μμ μκ·Ή μ μ λΉν΄ ICAM-1, VCAM-1 λ° I-selectin λΆμ λ°νμ μ μν λ³νλ₯Ό κ΄μ°°ν μ μμλ€.
3. 맀λ
κ· 47kDa νμμ 첨κ°νκ³ λ°°μν HDMEC νλ©΄μμ ICAM-1 λΆμ λ°νμ΄ μ¦κ°νμκ³ VCAM-1κ³Ό E-selectin λΆμ λ°νμ΄ κ΄μ°°λμμΌλ©°, λ°ν μμμ 맀λ
κ· 47kDa νμμ μ©λ μμ‘΄μ±μΌλ‘ μ¦κ°νμλ€.
4. 맀λ
κ· 47kDa νμμ 첨κ°νκ³ λ°°μν HDMEC νλ©΄μμ ICAM-1κ³Ό VCAM-1 λΆμλ°νμ 4μκ° νλΆν° μ¦κ°νμ¬ 24μκ°μ μ΅λμΉμ λλ¬ν ν 48μκ°κΉμ§ μ§μλμμΌλ©°, E-selectin λΆμ λ°νμ 1μκ° νλΆν° μ¦κ°νμ¬ 4μκ°μ§Έμ μ΅λμΉμ λλ¬νμλ€κ° 48μκ° νμλ λ°νμ κ΄μ°°ν μ μμλ€.
5. 맀λ
κ· 47kDa νμμ 첨κ°νκ³ λ°°μν HDMEC νλ©΄ ICAM-1κ³Ό VCAM-1 λΆμμ λ°ν μ¦κ°λ ν TNF-Ξ± ν체 λλ ν IL-1Ξ± ν체 μ²μΉμ μν΄ μ μνκ² μ΅μ λμλ€.
6. 맀λ
κ· 47kDa νμμ 첨κ°νκ³ λ°°μν HDMECμ λν T λ¦Όνꡬ μ μ°©μ λ°°μ 1μκ° νλΆν° μ¦κ°νκΈ° μμνμ¬ 4μκ° νμ μ΅λμΉμ λλ¬νμλ€κ° 48μκ°κΉμ§ μ§μλμλ€.
7. 맀λ
κ· 47kDa νμμ μν HDMECμ λν T λ¦Όνꡬμ μ μ°© μ¦κ°λ ν ICAM-1 ν체μ ν VCAM-1 ν체 μ²μΉμ μν΄ μ μνκ² μ΅μ λμλ€.
8. 맀λ
κ· 47kDa νμμ μν HDMECμ λν T λ¦Όνꡬμ μ μ°© μ¦κ°λ ν TNF-Ξ± ν체 λλ ν IL-1Ξ± ν체 μ²μΉμ μν΄ μ μνκ² μ΅μ λμλ€.
μ΄μμ κ²°κ³Όλ‘ λ§€λ
κ· κ³Ό 맀λ
κ· 47 kDa νμμ΄ μΈμ²΄ μ§νΌ λ―ΈμΈνκ΄ λ΄νΌμΈν¬ νλ©΄ ICAM-1,VCAM-1 λ° E-selectin λΆμ λ°νμ λ³νλ₯Ό μ λνκ³ T λ¦Όνꡬ μ μ°©μ μ‘°μ ν¨μΌλ‘μ¨ λ§€λ
μ λ©΄μνμ λ°λ³κΈ°μ μ κ΄μ¬ν κ²μΌλ‘ μκ°λλ©° μ΄ κ³Όμ μ νκ΄ λ΄νΌμΈν¬λ‘λΆν° μμ±λ TNF-Ξ±μ IL-1Ξ±κ° κ΄μ¬ν κ²μΌλ‘ μ¬λ£λλ€.
[μλ¬Έ]
Syphilis is a chronic, systemic sexually transmitted disease caused by the spirochetal bacterium Treponema pallidum subsp. pallidum(T. pallidum) with clinical features including various cutaneous lesions and systemic involvement. Histopathologically, perivasculitis and endothelial cell abnormalities are observed. In inflammatory and immune reactions, vascular endothelial cells act as key effecters. In such reactions the binding of leukocytes to endothelial cells is governed by the expression of cell adhesion molecules such as intercellular cell adhesion molecule-1(ICAM-1), vascular adhesion molecule-1 (VCAM-1) and I-selectin.
Their expressions are regulated by biological response modifiers and the resulting regulation of the binding of inflammatory cells plays an important role in determining the progression of acute and chronic inflammatory responses. Syphilitic lesions are induced net only by virulent T. pallidum but also immune reaction to the antigen of T. pallidum. It has been suggested that the T. pallidum-specific 47 kDa lipoprotein may play an important role in the pathogenesis of syphilis.
The present study utilized the immunofluorescence flow cytometry and the enzyme-linked immunosorbent assay to observe the changes in the expressions of ICAM-1, VCAM-1, and E-selectin on human dermal microvascular endothelial cells(HDMEC) following incubation with either virulent T. pallidum or the 47 kDa antigen. For the evaluation of the ability of adhesion molecules to mediate T lymphocytes' adhesion to HDMEC, the binding assay of T lymphocytes to HDMEC has been performed after stimulation of HDMEC with the 47 kDa antigen.
1. Expression of ICAM-1 on HDMEC increased significantly after stimulation with virulent T. pallidum and those of VCAM-1 and E-selectin were also induced. The expressions increased in a dose dependent manner with increasing cell number of T. pallidum.
2. Expressions of ICAM-1, VCAM-1 and E-selectin on HDMEC did not change after stimulation with non-pathogenic treponemes such as T. phagedensis, T. refringens, and T. denticola or heat-in-activated T. pallidum.
3. Expression of ICAM-1 on HDMEC increased significantly after stimulation with the 47 kDa antigen and those of VCAM-1 and E-selectin were also induced. The expressions increased in a dose dependent manner with increasing concentration of the 47 kDa antigen.
4. After stimulation with 47 kDa antigen the expressions of ICAM-1 and VCAM-1 on HDMEC increased significantly at 4 hours, reaching a peak at 24 hours and persisted until 48 hours. Expression of E-selectin was induced at 1 hour after stimulation
with a peak at 4 hours, but was not detectable after 48 hours.
5. Expressions of ICAM-1 and VCAM-1 on HDMEC after stimulation with the 47 kDa antigen decreased significantly by treatments with anti-TNF-Ξ± antibody or anti-lL- 1Ξ± antibody.
6. After stimulation with the 47 kDa antigen adherence of T lymphocytes to HDMEC increased significantly at 1 hour with a peak at 4 hours and persisted until 48 hours.
7. Adherence of T lymphocytes to HDMEC after stimulation with the 47 kDa antigen decreased significantly by treatment with anti-ICAM-1 antibody, anti-VCAM-1 antibody, anti-TNF-Ξ± anti-body or anti-IL- 1Ξ± antibody.
These data show that virulent T. pallidum or T. pallidum-specific 47 kDa antigen are capable of stimulating HDMEC to increase the expression of ICAM-1, VCAM-I and E-selectin on their membranes and thereby to promote adherence of T lymphocytes. The whole process may play an important role in the immunopathogenesis of syphilis and it is likely that TNFr and IL-1Ξ± are involved.restrictio
A study on Arabidopsis ABC transporters that participate on the deposition of pollen surface lipids
DoctorPollen surface is covered with pollen wall and coat, comprising of various lipophilic materials. These lipidic structures are important for pollen development as well as the protection of the pollen against external stresses, which are necessary for successful plant reproduction. The synthesis of their precursors in the tapetum, which is nourishing cells for pollen development, was unraveled by recent reports on the identification of the enzymes involved in that process. However, the mechanisms underlying the transport of these lipid materials from the tapetum onto pollen surface remain elusive. I hypothesized that ABCG transporters are good candidates for such function, as they are well known with their involvement in the transport of surface lipids. Here, I identified 3 Arabidopsis ABCG transporters, ABCG26, ABCG9 and ABCG31, which function in this process.ABCG26 was first isolated by drastically reduced seed production of two independent knockout mutant plants, which was complemented by expression of ABCG26 driven by its native promoter. The severely reduced fertility of the abcg26 mutants was caused by a failure to produce mature pollens. Defective pollen development in the mutant was initially observed at pollen wall developmental stage, i.e. the reticulate pattern of the exine of wild-type microspores was absent in abcg26 microspores at the vacuolate stage, and the vast majority of the mutant pollen degenerated thereafter. ABCG26 was expressed specifically in tapetal cells at the early vacuolate stage of pollen development. It was also highly co-expressed with genes encoding enzymes required for sporopollenin precursor synthesis, i.e. CYP704B1, ACOS5, MS2 and CYP703A2. The tapetal cells of abcg26 accumulated numerous vesicles and granules, which was also observed in two other mutants with defects in pollen wall deposition (nef1 and dex1). ABCG26 was localized to the plasma membrane. Taken together, these results suggest that ABCG26 plays a crucial role in the transfer of sporopollenin lipid precursors from tapetal cells to anther locules, facilitating exine formation on the pollen surface.Next, I searched for ABCG transporter genes that are highly expressed in anther to find candidate transporters involved in transport of pollen surface lipids. Using in silico microarray database, together with quantitative reverse transcriptase-PCR and promoter-GUS assays, I found that ABCG9 and ABCG31 were highly expressed in anthers and that the two genes exhibited a strong co-expression. Vital staining of pollens of abcg9 abcg31 double knockout plants revealed that half of them were non-viable. When exposed to air, many of the mutant pollens were shriveled and collapsed. When exposed to a cold shock during the flowering period, abcg9 abcg31 plants could not produce as many seeds as the wild type or the single knockout mutants. Electron microscopic observation of the pollen coat revealed that the pollen coat of the mutant was not fully-filled, and contained many vesicular or linear, electron-translucent structures. The extensive analyses of lipid composition of the pollen revealed that steryl glucosidesglycosides were reduced to about half in the abcg9 abcg31 pollen without any changes in the steryl ester and free sterol contents. Pollens of ugt80A2 ugt80B1, a mutant deficient in the steryl glucosidesglycosides synthesis, were similarly reduced in their viability, and often collapsed when exposed to air. Together, these results indicate that steryl glucosidesglycosides are one of the important materials for pollen fitness and that the two ABC transporters contribute to the accumulation of this class of sterols on pollen surface.Despite the huge number of ABC transporters of plants, there are few researches on their function in the pollen yet. On the hypothesis that ABCG transporters may be involved in the pollen surface lipid transport, similarly as several other members already studied for their functions in the cuticular lipid formation, I screened all ABCG transporters by observing the mutant phenotypes and using in silico microarray databases to find candidates for the transport of pollen surface lipids. By this screening, I isolated 3 ABCG transporters working in this process, and elucidated the function of ABCG26 in pollen wall, and that of ABCG9 and ABCG31 in pollen coat formation. In addition to unraveling the transport mechanisms for the deposition of pollen surface lipids, my study introduced a new aspect of functions of ABC transporters in pollen development and its proper function. Furthermore, I showed the analogy of the functions of the ABCG transporters for the formation of the surface lipids in different tissues. This analogy will help to identify more ABCG proteins with similar activities, and also synergistically improve our understanding of the pollen surface lipids and the cuticular lipids
Concurrent Validity of the Swallowing Monitoring & Assessment Protocol for the Elderly
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