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Carla B. Green is an American neuroscientist and professor of neuroscience at the University of Texas Southwestern Medical Center.

Background
Carla Green graduated from Missouri State University in 1984 and obtained her Ph.D. at the University of Kansas Medical Center in 1991. She worked on circadian rhythms in Xenopus as a postdoctoral fellow under Joseph Besharse, and upon completion of her fellowship in 1997, joined the Department of Biology at the University of Virginia to continue her research on circadian rhythms. In 2009, Green moved her lab to the Department of Neuroscience at the University of Texas Southwestern Medical Center.

Research contributions
Green's research concerns the molecular mechanisms involved in circadian rhythms. Her lab has three primary focuses: the study of Nocturnin, the role of circadian rhythms in regulating metabolic homeostasis, and the role of Cryptochrome proteins as repressors in circadian clocks.

Nocturnin
One focus of the Green Lab is research on the regulation and function of the circadian deadenylase Nocturnin (Noc, gene name; Ccrn4l). Noc encodes a deadenlyase, which is a polyA-specific ribonuclease that shortens polyA tails from mRNAs transcripts that have been translocated into the cytoplasm. There are 11 deadenylases in mammals with functions ranging from bone formation to the overall growth of organisms and belong two two superfamilies, DEDD (Asp-Glu-Asp-Asp) and EEP (Exonucleases, Endonucleases, Phosphates).

In a 2015 study, The Green Lab investigated the role of Noc in mice. Noc belongs to the second superfamily, EEP, and is unique in that it is the only deadenylase that possesses a rhythmic expression pattern controlled by the biological clock. Additionally, loss of Noc (Noc KO) results in mice who do not have reduced food intake, or increased activity, but are resistant to diet-induced obesity and hepatic steatosis. Green hypothesized that Noc uses its enzymatic activity on a specific subset of transcripts to shorten their poly(A) tail length, so a loss of this regulation would lead to observed features in Noc KO mice. They used a genome-wide screen they called Poly(A)adenylome analysis to determine the poly(A) tail lengths in Noc KO mouse liver. They found that most of the transcripts acted upon by Noc in the liver affect ribosome function and oxidative phosphorylation, which did not fit the functions expected. They concluded that Noc therefore operates either through a novel pathway or indirectly to control mRNA metabolism that eventually contribute to the characteristics seen in Noc KO mice.

Metabolic homeostasis
Green’s research has expanded the scientific understanding of the role of circadian rhythms in metabolic homeostasis. In 2012, Green and Joseph Takahashi examined the ability of central and peripheral circadian clocks in homeothermic mammals to entrain to environmental signals. Green and Takahashi observed that although the circadian clocks of individual cells were susceptible to entrainment by temperature cycles, intercellular coupling of suprachiasmatic nucleus (SCN) neurons made the SCN resistant to temperature changes, allowing it to regulate the body temperature of homotherms, making them resistant to external temperature changes. They also observed that peripheral circadian clocks were able to entrain to food-related cues, enabling mammals to anticipate feeding times, demonstrated by adjustments in daily rhythms such as activity and body temperature.

Cryptochrome proteins
Cryptochrome proteins (CRYs) are transcription repressors that are a necessary part of the circadian clock. Cryptochromes have a critical role in the mechanism of the circadian clock by forming a complex with Period protein (PER). Together, CRY and PER repress the activity of CLOCK and BMAL1, the proteins that activate expression of genes encoding. The Green Lab is interested in the two types of cryptochrome proteins in mammals, CRY1 and CRY2. The two proteins have similar structures but opposing roles in regulation of the circadian clock. Loss of CRY1 results in short periods and loss of CRY2 results in long periods. The elimination of CRY1 and CRY2 proteins causes organisms to become arrhythmic.

Post-translational modifications of the CRY proteins also appear to play an important role in determining the period length of a circadian rhythm. In 2013, Carla Green and colleagues identified a phosphorylation site, serine 588, in the C-terminal of a mouse CRY1. This site influences the period of the circadian rhythm depending on its phosphorylation status. Serine 588 on the C-terminal of CRY1 is regulated by a DNA-dependent protein kinase (DNA-PKcs). The phosphorylation of serine 588 stabilizes CRY1 protein, hence it prevents CRY1 degradation. The DNA-PK regulated phosphorylation of serine 588 also resulted in circadian rhythms with abnormally long periods. DNA-PK is also involved with DNA repair, so Green concluded that DNA-PK’s interaction with the circadian clock may be linked to a protective mechanism to prevent DNA damage from light and radiation. This research also revealed the importance of CRY1 C-terminal tail which has inconclusive data regarding its interaction to the circadian clock.