The Experts below are selected from a list of 6 Experts worldwide ranked by ideXlab platform
Ying Xia - One of the best experts on this subject based on the ideXlab platform.
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Loss of MAP3K1 enhances proliferation and apoptosis during Retinal development.
Development (Cambridge England), 2011Co-Authors: Maureen Mongan, Jingcai Wang, Hongshan Liu, Yunxia Fan, Chang Jin, Winston Whei-yang Kao, Ying XiaAbstract:Precise coordination of progenitor cell proliferation and differentiation is essential for proper organ morphogenesis and function during mammalian development. The mitogen-activated protein kinase kinase kinase 1 (MAP3K1) has a well-established role in anterior eyelid development, as Map3k1-knockout mice have defective embryonic eyelid closure and an `eye-open at birth' (EOB) phenotype. Here, we show that MAP3K1 is highly expressed in the posterior of the developing eye and is required for Retina development. The MAP3K1-deficient mice exhibit increased proliferation and apoptosis, and Muller glial cell overproduction in the developing Retinas. Consequently, the Retinas of these mice show localized rosette-like arrangements in the outer nuclear layer, and develop abnormal vascularization, broken down Retinal pigment epithelium, photoreceptor loss and early onset of Retinal degeneration. Although the Retinal defect is associated with increased cyclin D1 and CDK4/6 expression, and RB phosphorylation and E2F-target gene upregulation, it is independent of the EOB phenotype and of JNK. The Retinal developmental defect still occurs in knockout mice that have undergone tarsorrhaphy, but is absent in compound mutant Map3k1(+/ΔKD)Jnk1(-/-) and Map3k1(+/ΔKD)Jnk(+/-)Jnk2(+/-) mice that have EOB and reduced JNK signaling. Our results unveil a novel role for MAP3K1 in which it crosstalks with the cell cycle regulatory pathways in the prevention of Retina Malformation and degeneration.
Christopher A. Emerling - One of the best experts on this subject based on the ideXlab platform.
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Regressed but Not Gone: Patterns of Vision Gene Loss and Retention in Subterranean Mammals.
Integrative and comparative biology, 2018Co-Authors: Christopher A. EmerlingAbstract:Regressive evolution involves the degradation of formerly useful traits as organisms invade novel ecological niches. In animals, committing to a strict subterranean habit can lead to regression of the eyes, likely due to a limited exposure to light. Several lineages of subterranean mammals show evidence of such degeneration, which can include decreased organization of the Retina, Malformation of the lens, and subcutaneous positioning of the eye. Advances in DNA sequencing have revealed that this regression co-occurs with a degradation of genomic loci encoding visual functions, including protein-coding genes. Other dim light-adapted vertebrates with normal ocular anatomy, such as nocturnal and aquatic species, also demonstrate evidence of visual gene loss, but the absence of comparative studies has led to the untested assumption that subterranean mammals are special in the degree of this genomic regression. Additionally, previous studies have shown that not all vision genes have been lost in subterranean mammals, but it is unclear whether they are under relaxed selection and will ultimately be lost, are maintained due to pleiotropy or if natural selection is favoring the retention of the eye and certain critical underlying loci. Here I report that vision gene loss in subterranean mammals tends to be more extensive in quantity and differs in distribution from other dim light-adapted mammals, although some committed subterranean mammals demonstrate significant overlap with nocturnal microphthalmic species. In addition, blind subterranean mammals retain functional orthologs of non-pleiotropic visual genes that are evolving at rates consistent with purifying selection. Together, these results suggest that although living underground tends to lead to major losses of visual functions, natural selection is maintaining genes that support the eye, perhaps as an organ for circadian and/or circannual entrainment.
Maureen Mongan - One of the best experts on this subject based on the ideXlab platform.
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Loss of MAP3K1 enhances proliferation and apoptosis during Retinal development.
Development (Cambridge England), 2011Co-Authors: Maureen Mongan, Jingcai Wang, Hongshan Liu, Yunxia Fan, Chang Jin, Winston Whei-yang Kao, Ying XiaAbstract:Precise coordination of progenitor cell proliferation and differentiation is essential for proper organ morphogenesis and function during mammalian development. The mitogen-activated protein kinase kinase kinase 1 (MAP3K1) has a well-established role in anterior eyelid development, as Map3k1-knockout mice have defective embryonic eyelid closure and an `eye-open at birth' (EOB) phenotype. Here, we show that MAP3K1 is highly expressed in the posterior of the developing eye and is required for Retina development. The MAP3K1-deficient mice exhibit increased proliferation and apoptosis, and Muller glial cell overproduction in the developing Retinas. Consequently, the Retinas of these mice show localized rosette-like arrangements in the outer nuclear layer, and develop abnormal vascularization, broken down Retinal pigment epithelium, photoreceptor loss and early onset of Retinal degeneration. Although the Retinal defect is associated with increased cyclin D1 and CDK4/6 expression, and RB phosphorylation and E2F-target gene upregulation, it is independent of the EOB phenotype and of JNK. The Retinal developmental defect still occurs in knockout mice that have undergone tarsorrhaphy, but is absent in compound mutant Map3k1(+/ΔKD)Jnk1(-/-) and Map3k1(+/ΔKD)Jnk(+/-)Jnk2(+/-) mice that have EOB and reduced JNK signaling. Our results unveil a novel role for MAP3K1 in which it crosstalks with the cell cycle regulatory pathways in the prevention of Retina Malformation and degeneration.
Jingcai Wang - One of the best experts on this subject based on the ideXlab platform.
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Loss of MAP3K1 enhances proliferation and apoptosis during Retinal development.
Development (Cambridge England), 2011Co-Authors: Maureen Mongan, Jingcai Wang, Hongshan Liu, Yunxia Fan, Chang Jin, Winston Whei-yang Kao, Ying XiaAbstract:Precise coordination of progenitor cell proliferation and differentiation is essential for proper organ morphogenesis and function during mammalian development. The mitogen-activated protein kinase kinase kinase 1 (MAP3K1) has a well-established role in anterior eyelid development, as Map3k1-knockout mice have defective embryonic eyelid closure and an `eye-open at birth' (EOB) phenotype. Here, we show that MAP3K1 is highly expressed in the posterior of the developing eye and is required for Retina development. The MAP3K1-deficient mice exhibit increased proliferation and apoptosis, and Muller glial cell overproduction in the developing Retinas. Consequently, the Retinas of these mice show localized rosette-like arrangements in the outer nuclear layer, and develop abnormal vascularization, broken down Retinal pigment epithelium, photoreceptor loss and early onset of Retinal degeneration. Although the Retinal defect is associated with increased cyclin D1 and CDK4/6 expression, and RB phosphorylation and E2F-target gene upregulation, it is independent of the EOB phenotype and of JNK. The Retinal developmental defect still occurs in knockout mice that have undergone tarsorrhaphy, but is absent in compound mutant Map3k1(+/ΔKD)Jnk1(-/-) and Map3k1(+/ΔKD)Jnk(+/-)Jnk2(+/-) mice that have EOB and reduced JNK signaling. Our results unveil a novel role for MAP3K1 in which it crosstalks with the cell cycle regulatory pathways in the prevention of Retina Malformation and degeneration.
Hongshan Liu - One of the best experts on this subject based on the ideXlab platform.
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Loss of MAP3K1 enhances proliferation and apoptosis during Retinal development.
Development (Cambridge England), 2011Co-Authors: Maureen Mongan, Jingcai Wang, Hongshan Liu, Yunxia Fan, Chang Jin, Winston Whei-yang Kao, Ying XiaAbstract:Precise coordination of progenitor cell proliferation and differentiation is essential for proper organ morphogenesis and function during mammalian development. The mitogen-activated protein kinase kinase kinase 1 (MAP3K1) has a well-established role in anterior eyelid development, as Map3k1-knockout mice have defective embryonic eyelid closure and an `eye-open at birth' (EOB) phenotype. Here, we show that MAP3K1 is highly expressed in the posterior of the developing eye and is required for Retina development. The MAP3K1-deficient mice exhibit increased proliferation and apoptosis, and Muller glial cell overproduction in the developing Retinas. Consequently, the Retinas of these mice show localized rosette-like arrangements in the outer nuclear layer, and develop abnormal vascularization, broken down Retinal pigment epithelium, photoreceptor loss and early onset of Retinal degeneration. Although the Retinal defect is associated with increased cyclin D1 and CDK4/6 expression, and RB phosphorylation and E2F-target gene upregulation, it is independent of the EOB phenotype and of JNK. The Retinal developmental defect still occurs in knockout mice that have undergone tarsorrhaphy, but is absent in compound mutant Map3k1(+/ΔKD)Jnk1(-/-) and Map3k1(+/ΔKD)Jnk(+/-)Jnk2(+/-) mice that have EOB and reduced JNK signaling. Our results unveil a novel role for MAP3K1 in which it crosstalks with the cell cycle regulatory pathways in the prevention of Retina Malformation and degeneration.